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Psychology 211 Review
3/14/2012 3:22:00 PM
Chapter 1
dualism: belief that the mind and body are separate, Descartes
monism: belief that the universe is everything that’s physically there, that
the mind emerges from the workings of the physical brain
unilateral neglect emerges from damage to the right parietal lobe, causing
left-sided neglect
experimental ablation: method of studying the brain by removing certain
parts of animals’ brains and then observing their behavior
Hemholtz discovered that neural conduction was slower than conduction
through wires, by which electricity travels at the speed of light

due to the nature of neurons, level of myelination, size of axons,
etc.
functionalism: perspective of study emphasizing the usefulness of functions
of the characteristics of living organisms
 theory of natural selection was developed around the discovery and
study of these functions
evolution of the human brain seemed to have a lot to do with its
development slowing, called neoteny, allowing the brain to adapt to the
environment and permitting a much greater deal of learning
Chapter 2
somatic nervous system: interacts with external environment
autonomic nervous system: regulates the body internally
sensory neurons: neurons that carry information from the sensory receptors
to the brain (and, to a lesser extent, in the other direction)
motor neurons: neurons that carry information from the brain to muscles
(and, to a lesser extent, in the other direction)
interneurons: neurons with no axon but many dendrites that integrate
information from sensory/motor neurons
 local interneurons: co-ordinate information between local nearby
units of neurons
 relay interneurons: integrate the information from local
interneurons in two different areas
multipolar neurons: most common kind of neuron, have one axon but
multiple dendrites
bipolar neurons: usually sensory, have one axon and one dendrite
unipolar neurons: usually detect sensory events in the skin, have one
projection from the soma that splits in two, branches outside of the central
nervous system are dendrites and those inside of it end in terminal buttons
ncRNA: non-coding RNA, binds to protein and thereby affects gene
expression
axoplasmic transport: the means by which materials are transported
between the soma and terminal button, consisting of the active transport of
those materials through microtubules that run the length of the axon
 anterograde transport: the movement from the soma to the
terminal buttons

retrograde transport: the movement from the terminal buttons to
the soma (slower)
astrocytes: star-shaped glial cells that provide physical support and
nurishment to neurons, clean up debris in the brain, and regulate the
concentration of substances in neurons’ extra-membrane fluid
 in physically surrounding the neurons, they serve as a conduit
between the neurons and blood vessels, as well as to isolate
synapses from one another so neuronal messages don’t get
confused
oligodendrocytes: glial cells that make up the myelin sheath in the central
nervous system
nodes of Ranvier: the gaps between strips of myelin sheath
 saltatatory conduction: the jumping of the action potential from one
node of Ranvier to the next by sodium ions rushing in at each node
and thereby retriggering the potential
o reduces the amount of sodium ions that need to enter the cell
and therefore eventually be removed
o allows conduction to be faster and prevents the action
potential from spreading to other neurons
microglia: smallest glial cells, serve to clean up debris and as the brain’s
immune system
Schwann cells: glial cells that make up the myelin sheath in the peripheral
nervous system, also help to digest dying axons and form a cylinder to guide
the re-growth of new axons and allow them to establish connections with
muscles and sensory organs

oligodendrocytes don’t do this in the central nervous system,
astrocytes form around where dead neural tissue was and send out
signals preventing new growth
blood-brain barrier: selectively-permeable membrane between the brain and
its surrounding fluid and the rest of the body through which substances only
pass by the means of protein transporters, necessary because of the delicate
composition of the extra-cellular fluid in the brain as well as its vulnerability
to toxins
 weaker around the area postrema, responsible for the vomiting
reflex, allowing the detection of toxins
oscilloscope: voltmeter that’s sensitive enough to transcribe a neuron’s
electrical activity
wire electrode: placed in the fluid surrounding an axon and stimulated with
electrical activity to thereby stimulate an action potential
glass microelectrode: inserted into the axon to record its activity and
transmit that information to an oscilloscope
resting potential: the electric charge of a neuron’s membrane in the absence
of any action potentials (difference between inner- and outer-membrane
fluid), -70 mV
threshold of excitation: the level of depolarization necessary for an axon to
produce an action potential
electrolytes: substances that split into two components with opposite
charges (called ions) when dissolved in water
electrostatic pressure: the forces produced by same charges attracting and
opposite charges repelling
A-: organic anion, located inside the cell because the membrane is
impermeable to it
K+: located inside the cell, diffusion would force it out but electrostatic
pressure forces it in
Cl-: located outside the cell, diffusion would force it in but electrostatic
pressure keeps it out
Na+: located outside the cell, diffusion and electrostatic pressure both push
it in so the sodium-potassium pump transports out the Na+ that leaks in
through the membrane, which is also not very permeable to it
action potential occurs when sodium channels open and the membrane
becomes extremely permeable to Na+, causing a depolarization as Na+
rushes into the cell, reaching a peak of 30 mV and then a brief
hyperpolarization as the membrane becomes even more permeable to K+
and it rushes out, and then a return to the resting membrane potential
voltage-dependent ion channels: ion channels that open when the
membrane reaches a certain voltage level
 sodium channels close as the action potential reaches its peak
 potassium channels close as the membrane potential re-approaches
its resting level
axons have the capacity to carry action potentials in either direction, but it’s
usually away from the soma because that’s where the action potential is
generally generated
axodendritic synapses: synapses between axons and dendrites, either on the
dendrites’ smooth surface or its spine
axosomatic synapses: synapses between an axon and a soma
axoaxonic synapses: synapses between two axons
release zone: the part of the terminal button where vesicles filled with
neurotransmitters are released into the synaptic cleft
postsynaptic potential: the potential generated by the release of a
neurotransmitter that affects an axon’s firing rate caused by the binding of
neurotransmitters to neurotransmitter-dependent ion channels, causing
them to open or close (depending on the ion channel)
neurotransmitters are released in response to an influx of Ca2+, caused by
an opening of calcium channels in response to the depolarizing action
potential
ionotropic receptor: a kind of neurotransmitter receptor that opens in direct
response to a neurotransmitter binding to it, produces faster potentials
metabotropic receptor: a kind of neurotransmitter receptor that opens in
response to the neurotransmitter binding to a G protein, activating an
enzyme that causes the production of the second messenger, one of several
chemicals (one is cAMP) that attaches to ion channels after traveling through
the cytoplasm and causes them to open, produces longer-lasting potentials
 second messengers can have other effects on the cell aside from
helping to open the ion channel
excitatory postsynaptic potential (EPSP): the postsynaptic potential that
occurs when a receptor controlling a sodium or calcium channel is stimulated
to open

can be neutralized by the opening of chlorine channels, which will
flood into a cell that’s been depolarized and thereby return its
membrane potential to the resting level
 when calcium channels open, they also stimulate the production of
certain enzymes, which causes some other changes to the cell
inhibitory postsynaptic potential (IPSP): the postsynaptic potential that
occurs when a receptor controlling a potassium channel is stimulated to
open
reuptake: the removal of neurotransmitters from the synaptic cleft by
special transporter molecules after the receptors have been exposed to them
enzyme deactivation: a way of ending a postsynaptic potential by means of
an enzyme that takes apart the neurotransmitter, used only for acetylcholine
axon hillock: the place at the base of the axon, near the soma, where the
postsynaptic potentials are integrated and the action potential is stimulated
or not, depending on the overall charge
autoreceptors: metabotropic neurotransmitter receptors that respond to
neurotransmitters released by their own cell, which are involved in
regulating the synthesis and release of neurotransmitters
presynaptic inhibition: activity at an axoaxonic synapse that decreases
neurotransmitter release
presynaptic facilitation: activity at an axoaxonic synapse that increases
neurotransmitter release
axoaxonic synapses don’t contribute to neural integration, but instead play a
role in regulating the amount of neurotransmitter released
neuromodulators: chemicals (usually peptides) released that travel farther
and more widely than neurotransmitters, therefore having more widespread
effects over numerous neurons
target cells: cells that respond to a specific hormone, stimulated by the
hormone binding to metabotropic receptors in the cell’s membrane
steroids: fat-soluble molecules that communicate by binding directly to the
nucleus of the cell
Chapter 3
rostral: towards the beak (front of the face and body in humans), caudal:
back of the head and feet
dorsal: towards the tail (top of the head and back in humans), ventral: front
of head and belly
meninges: protective layers surrounding the brain and spinal cord,
consisting of three parts
 dura mater: tough and thick outermost layer of the meninges
 arachnoid membrane: spongy middle layer of the meninges
 subarachnoid space: space between the arachnoid membrane and
the pia mater, filled with cerebrospinal fluid
 pia mater: network of blood vessels that lies closest to the brain
and spinal cord
lateral ventricles: large and lateral-most ventricles, connected by the third
ventricle
third ventricle: located on the midline of the brain, separated in two by
neural tissue
fourth ventricle: located near the cerebellum and connected to the third
ventricle by the cerebral aqueduct
choroid plexus: rich blood supply near each ventricle that constantly
replenishes its cerebrospinal fluid supply
old cerebrospinal fluid leaves the ventricles through the subarachnoid space
near the fourth ventricle, where it’s re-absorbed into the blood through the
arachnoid granulations by means of the superior sagittal sinus
obstructive hydrocephalus: the swelling of the brain resulting from the
blocking of the draining of CSF, can be fatal if not operated on
ventricular zone: the zone of cells in the earliest stages of developing into
the central nervous system, consisting of progenitor cells, which divide at
first into more progenitor cells (symmetrical division) and then eventually
differentiate (asymmetrical division)
longer period of symmetrical and asymmetrical division in humans could
account for humans’ larger brain size and unique cognitive characteristics
 -catenin: protein involved in regulating cell division and the length
of symmetrical division, thought that a mutation in this protein
could’ve led to the increased length of symmetrical and
asymmetrical divisions and thereby to increased brain size
radial glia: the first type of neural cell that develops during asymmetrical
division, which remain in the ventricular zone but extend projections that
attach to the pia mater
Cajal-Retzius (C-R) cells: cells that rest just next to the pia mater
the longer asymmetrical division lasts, the farther new neuronal cells have to
travel, meaning the process gets exponentially slower
once developing neurons reach their designated location, they begin to form
connections with surrounding cells, determining which cells they connect to
based on the chemicals that they release
three divisions are evident in the neural tube: forebrain (later divides into
the telencephalon and diencephalon), midbrain (mesencephalon), and
hindbrain (metencephalon and myelencephalon)
telenephalon: cerebral cortex, basal ganglia and limbic system
association areas located farther from a certain primary sensory cortex
integrate more information from more varied sensory modalities
left hemisphere is better at analysis of information, processing serial events,
and controlling behavior
right hemisphere is better at the integration of information
limbic cortex: part of the cerebral cortex located most medially
neocortex: rest of the cerebral cortex (frontal, parietal, temporal, and
occipital lobes)
septum: structure attached to the corpus callosum and fornix, with
connections to the amygdala and hippocampus
fornix: connects the hippocampus with other parts of the brain, like the
mammillary bodies
mammillary bodies: protrusions on the base of the brain, includes parts of
the hypothalamus
basal ganglia: group of subcortical structures including the putamen, globus
pallidus, and caudate nucleus that lie below the anterior part of the lateral
ventricles, important for co-ordinated movement
 putamen: band on axons in the middle of the caudate nucleus


caudate nucleus: C-shaped structure
globus pallidus: receives input from the striatum (putamen and
caudate nucleus)
diencephalon: area surrounding the third ventricle, in between the
telencephalon and the mesencephalon, constitutes the thalamus and
hypothalamus
lateral geniculate nucleus (LGN): part of the thalamus that receives
information from the eye and superior colliculus and sends it to the striate
cortex
medial geniculate nucleus: part of the thalamus that receives information
from the ear and sends it to the primary auditory cortex
ventrolateral nucleus: part of the thalamus that relays information from the
cerebellum to the primary motor cortex
hypothalamus: responsible for basic functions necessary for survival, located
on top of the pituitary gland, has neurosecretory cells that secrete hormones
that stimulate the pituitary gland to then secrete hormones and release
them throughout the body
midbrain/mesencephalon: area surrounding the cerebral aqueduct, consists
the tectum and tegmentum
tectum: consists the superior and inferior colliculi, located on the base of the
brain stem
 superior colliculus: involved in visual processing
 inferior colliculus: involved in auditory processing
tegmentum: part of the mesencephalon below the tectum, consists the
periaqueductal grey matter, the red nucleus, the substantia nigra, and the
ventral tegmental area
 reticular formation: located between the medulla and the midbrain,
responsible for relaying information to the cortex, thalamus, and
spinal cord, and for sleep and arousal, attention, and movement
 periaqueductal grey matter: grey matter surrounding the cerebral
aqueduct, important for species-specific behavior
 red nucleus: relays motor information to the cortex and cerebellum
 substantia nigra: relays information to the basal ganglia
hindbrain: consists the metencephalon and myelencephalon, area
surrounding the fourth ventricle
metencephalon: consists the pons and cerebellum
 cerebellum: important for smooth and co-ordinated complex
movements
 pons: bulge in the brain stem between the mesecenphalon and
medulla oblongata, contains part of the reticular formation, relays
information from the cortex to the cerebellum
myelencephalon: consists the medulla oblongata, which sits just on top of
the spinal cord, contains part of the reticular formation, regulates vital bodily
functions
diencephalon: thalamus and hypothalamus
mesencephalon: tectem and tegmentum
metencephalon: cerebellum and pons
myelencephalon: medulla oblongata
Chapter 4
sites of action: sites where drug molecules interact with cells in the body
most significant drugs act on the central nervous system
intravenous (IV) injection: injection into the bloodstream, takes a few
seconds to reach the brain
intraperitoneal (IP) injection: injection into the space surrouding the
stomach, used for animals, not as fast as an IV injection
intramuscular (IM) injection: injection into a large muscle, enters the
bloodstream through the muscle’s capillaries, can be released slowly if
combined with a chemical that constricts blood vessels
subcutaneous (SC) injection: injection under the skin, good for small
amounts of drug, can be slow-releasing if dissolved in vegetable oil
drugs that won’t dissolve in the stomach’s acid can be administered orally or
sublingually
route from lungs to brain is short, effectiveness of inhalation
snorting drugs is topic administration to the nose’s mucus membrane
intracerebral administration: injection of drug directly into the brain
intracerebroventricular (ICV) administration: injection of the drug into a
cerebral ventricle
speed that drugs get to the brain can depend on lots of different variables

lipid solubility: the more lipid soluble, the more easily they’ll get
through the blood-brain barrier
 depot binding: binding to body tissues or blood proteins, delays its
passage to the brain and can prolong its effects
dose-response curve: curve plotting the dosage of a drug against its effect,
plateaus at a certain point, after which increasing the dose has no more
effect

margin of safety: the distance between the dose-response curve of
the drug’s desired and undesired effects, showing the dose at which
the drug can safely be administered
 therapeutic index: the ratio of the dose at which the drug produces
the desired effect in 50% of test animals, and the dose at which the
drug produces a toxic effect in 50% of test animals, higher the
number, the larger the margin of safety and therefore the less
likelihood of an overdose
 point of maximum effect: the plateau of the drug’s effectiveness
affinity: the ease with which a drug binds to a site of action and therefore
how effective it is, can vary for the same drug between different sites of
action
tolerance: the body’s attempt to compensate for the effects of the drug by
reducing the number of receptors or decreasing the effectiveness of binding
with the receptors the drug binds to
withdrawal: the negative reaction to stopping taking a drug due to the
body’s compensatory measures, resulting in the opposite of the normal
effect of the drug
sensitization: the body becomes more and more sensitive to the effects of a
drug with repeated use
agonist: a drug that enhances the effect of a neurotransmitter in any way
antagonist: a drug that inhibits the effect of a neurotransmitter in any way
presynaptic heteroreceptors: receptors seen at axoaxonic synapses that bind
with the neurotransmitters released by the other terminal button, and either
inhibit or facilitate the neurotransmitter release from the terminal button
they’re attached to by regulating calcium channels, which controls the
release of neurotransmitters in the pre-synaptic membrane
glutamate: amino acid, main excitatory neurotransmitter in the brain


NMDA receptor: ionotropic, has six binding sites, opens ion
channels letting in sodium as well as calcium, which promotes
structural changes that are important in forming new memories, ion
channel won’t open unless glycine binds in addition to glutamate
and the magnesium ion that’s normally bound to it isn’t bound,
which happens when the postsynaptic membrane is partially
depolarized
AMPA receptor: ionotropic
 kainite receptor: ionotropic
 metabotropic glutamate receptor: metabotropic
GABA: amino acid, main inhibitory neurotransmitter in the brain
 GABAA: ionotropic, controls a chloride channel and has five binding
sites, all barbiturates bind to one and serve as agonists
 GABAB: metabotropic, controls a potassium channel, can be a
postsynaptic receptor or an antagonist
 benzodiazepines are GABA agonists and reduce anxiety and induce
sleep
glycine: amino acid, inhibitory neurotransmitter in the lower parts of the
brain and spinal cord
 receptor is ionotropic and controls a chloride channel
aspartate: amino acid, excitatory neurotransmitter, but not as strongly
excitatory as glutamate
some terminal buttons release both GABA and glycine, which makes the
postsynaptic potential both long-lasting and rapid, because GABA stimulates
the metabotropic receptor and glycine stimulates the ionotropic one
acetylcholine (ACh): primary neurotransmitter in the peripheral nervous
system, responsible for all muscle movement and important for the
autonomic nervous system, made up of acetate and choline
 nicotinic receptors: ionotropic ACh receptor
o botox and curare both bind to these receptors and are
antagonists
 muscarinic receptors: metabotropic ACh receptor, more common in
the central nervous system
monoamines: dopamine, norepinephrine, epinephrine, and serotonin
 catecholamines: subclass of monoamines, dopamine,
norepinephrine, and epinephrine
L-DOPA: a pre-cursor to dopamine, injections of L-DOPA facilitate dopamine
production
dopaminergic systems: systems of the brain where dopaminergic neurons
are
 nigrostriatal system: neurons that project from the substantia
nigra to the striatum
o Parkinson’s emerges from a breakdown of functioning in this
system

mesolimbic system: neurons that project from the ventral
tegmental area to the limbic system, important for rewarding
behavior
 mesocortical system: neurons that project from the ventral
tegmental area to the prefrontal cortex
 all dopaminergic receptors are metabotropic
 cocaine and methylphenidate block dopamine and norepinephrine
reuptake
the noradrenergic system originates mostly in the pons, medulla oblongata,
and thalamus


norepinephrine is important for vigilance and attention
it’s released through axonal varicosities (swellings on the axons)
and not through terminal buttons
epinephrine is actually a hormone produced by the adrenal glands and
serves minor importance as a neurotransmitter in the brain
serotonin: neurotransmitter in the brain important for mood, eating, sleep,
arousal, and dreaming
 tryptophan is a precursor for it
 agonists that block its reuptake are important in treating mental
disorders
Chapter 5
experimental ablation: destroying a part of a test animal’s brain for the
purpose of research
excitotoxic lesions: lesions produced by injecting an excitatory substance
like kanic acid, which will kill the neuron by overexciting it, more specific
than lesions created by electricity
lesions can also by created by inserting an electrode insulated except for at
the tip and passing an electrical current through it, destroys everything in
the vicinity, including axons that pass through the area
sham lesions: a kind of placebo for creating lesions, make sure that the
procedure’s effects aren’t mistaken for the lesion’s effects, go through entire
procedure except for actually creating the lesion
temporary lesions: temporarily disrupting the brain activity in an area, can
be done by injecting muscimol, a GABA agonist, thereby inhibiting all action
potentials while the drug is in effect
stereotaxic surgery: the surgery method by which a lesion is inflicted,
making use of a stereotaxic apparatus to hold the animal’s head in place and
a stereotaxic atlas of the animal’s brain to know where to inject the drug,
precision of the lesion is inspected afterwards by looking directly at the
animal’s brain
 based around the bregma, the more rostral junction of the skull,
and the lambda, the more caudal junction
fixative: the substance the brain is placed in after the animal is killed to
preserve it, usually formalin, which stops the work of autolytic enzymes,
which would otherwise digest the brain, and hardens it
Nissl stain: stains the cell bodies of all cells
Golgi stain: all of some cells, done by injecting cells with salts, which then
diffuse throughout the entire cell (including the axons and dendrites)
transmission electron microscope: transmits very magnified and detailed
two-dimensional information
scanning electron microscope: transmits slightly less magnified information,
but in 3d
confocal laser scanning microscope: requires that the brain tissue be stained
but not necessarily into thin slices like the other kinds do
anterograde labeling method: used to trace the path from one structure to
another, by tracing a chemical (like the protein PHA-L) that’s taken up by
the dendrites and then axons
 immunocytochemicals: antibodies or antigens that attach to a
particular protein and therefore reveal where those proteins are in
the brain (and thereby the pathway of interest)
retrograde labeling method: used to trace the path backwards from a
particular structure, by injecting a chemical (like fluorogold) into the
terminal button, from where it’s taken up through the axon and transported
to the cell bodies
CT scans: x-rays of the brain
magnetic resonance imaging (MRI): use of a strong magnetic field that
causes certain molecules to orient in a certain way
diffusion tensor imaging (DTI): a kind of MRI scan that reveals the pathways
in the brain based on water flow
single-unit recording: a recording of the activity of a single neuron using a
microelectrode
macroelectrodes: record the activity of a large area of the brain, or of the
entire brain, can be inserted into the brain or placed on the scalp
electroencephalograms (EEGs): transcription of recorded brain activity taken
by the means of an electrode cap of macroelectrodes placed on the scalp
magnetoencephalography (MEG): transcription of the brain’s activities by
using very sensitive detectors of magnetic fields that measure the changes
in magnetic fields when an action potential occurs
2-DG: a radioactive chemical taken up by cells as though it’s glucose,
allowing tracing of metabolic activity
autoradiography: record of radioactive traces in the brain
positron emission tomography (PET) scans: measure of the brain’s activity
by tracing the positron emissions of a radioactive substance, like 2-DG, poor
spatial and temporal resolution
functional magnetic resonance imaging (fMRI): use of MRI technology over
time to track the position of oxygenated blood molecules, which orient
themselves differently than those that are deoxygenated
can stimulate the brain chemically using an excitatory substance, allowing
more selectivity in exciting only certain neurons, or electrically, which
unselectively excites everything in a certain area
microiontopheresis: transmission of substances (onto drugs) onto specific
neurons using a multibarreled micropipette and a microelectrode that
records the neuron’s activity
transcranial magnetic stimulation (TMS): neural stimulation using magnetic
fields, can only be used for neurons in the cerebral cortex, can stimulate the
activity in an area or inhibit it (depending on the strength of the magnetic
field)
channelrhodopsin-2 (ChR2): photosensitive protein found in green algae that
controls a sodium and calcium channel, that opens the channel and thereby
depolarizes the membrane when exposed to blue light
natronomonas pharaonis halorhodopsin (NpHR): photosensitive protein
found in bacteria that controls a chloride channel, that opens the channel
and thereby hyperpolarizes the membrane when exposed to yellow light
choline acetyltransferase (ChAT): enzyme that’s necessary for the
production of ACh, its presence therefore implies the secretion of ACh
in situ hybridization: tagging certain mRNA with a radioactive substance to
see where it showed up and therefore where the protein that it codes for is
microdialysis: method of analyzing extracellular fluid by inserting a small
tube with a solution in it similar to extracellular fluid so that any other
substances diffuse into it, can be used to look at the presence and/or
concentration of certain neurotransmitters
antisense oligonucleotides: modified RNA or DNA that will bind with mRNA
and stop it from producing a protein
Chapter 6
most sensory receptors don’t have axons, but form synapses with other
dendrites directly onto their somas
hue is the perceptual equivalent of wavelength, brightness is the perceptual
equivalent of intensity, and saturation is the perceptual representation of
how narrow the distribution of wavelengths is
 we perceive objects as white or black (without hue) if they reflect
the entire spectrum or none of the spectrum
sclera: the tough white outer coating of the eye
vergence movements: the coordinated movement of the eyes by the
extraocular muscles in order to keep the object of attention in corresponding
spots on both eyes
saccadic movements: the jerky movements of the eyes to explore a stimulus
pursuit movement: the smooth movement of the eyes to track a moving
target
birds have eyes that take up most of their heads, and two foveas, one
pointing ahead and one pointing to the side, also have more photoreceptors
on the top half of their retinas, making their sight looking down very good
but making it almost impossible for them to look up without turning their
heads sideways
bipolar cells: between the photoreceptor layer and the retinal ganglion cell
layer and transmits information between the two
ganglion cells: cells that integrate light information from the photoreceptors
and send that information to the brain through the optic nerve
photoreceptors: cells at the very back of the eye that react to light stimuli
 lamellae: thin membranes that are in the outer segment of the
photoreceptor, studded with photopigments
o photopigments: molecules made up of an opsin (a protein)
and a retinal (a lipid), rhodopsin in humans
when photopigments are exposed to light, they break
down into their components and change color, called
“bleaching”
inner segment of the photoreceptor is made up of the cell body and
an axon-like projection
dark current: the constant flow of glutamate that photoreceptors
emit when not exposed to a light stimulus due to cGMP holding the
ion channels open, dark current is cut off when the photopigment is
bleached and causes a chemical reaction with a G protein and an
enzyme that destroys cGMP, which hyperpolarizes the membrane



and thereby cuts off the flow of glutamate, this decrease in
glutamate depolarizes the membrane of the bipolar cell attached to
it, which had been being hyperpolarized by the glutamate binding
to inhibitory receptors, and the bipolar cell produces more
glutamate which depolarizes the ganglion cell and causes it to fire
more or less, depending on if the light stimulus was in the
excitatory or inhibitory part of its receptive field
horizontal and amacrine cells: cells that integrate photoreceptor information
laterally
lateral geniculate nucleus (LGN): receives visual information from the retina,
divided into six layers, layers 1 and 2 are magnocellular and receive
information from parasol ganglion cells (therefore the periphery) and layers
3-6 are parvocellular and receive information from midget ganglion cells
(therefore the fovea)
 konicellular sublayers: layers ventral to each of the magnocellular
and parvocellular layers
circadian rhythm is regulated by the hypothalamus
optic tectum and pretectal nuclei: responsible for controlling the muscles
that control eye movements, the ciliary muscles, and the muscles that
control the size of our pupil
ON/OFF cells: cells that respond with a sudden burst of excitation to a light
being turned on or off, project to the superior colliculus and help with visual
reflexes
ON cells: cells that respond more to light in the center and less to light in
the surround, important for detecting spots that are brighter than the
background, rods are entirely ON cells
S, M, and L cones: photoreceptors that respond especially to a certain
wavelength of light (short, medium or long wavelength), depending on what
kind of opsin they have in their photopigments
 trichromacy theory is supported by the existence of these different
kinds of photoreceptors, seems to be true at the level of the retina
 rely on all three kinds of cones to perceive color, if just relying on
one kind of cone, a low response could indicate a light at a
wavelength at either end of its spectrum, and a high response could
indicate high saturation or high intensity, integration of the
information from all three provides more information
protanopia: incapacity to distinguish between red and green, L
photoreceptors have photopigments with M opsin in them
deuteranopia: incapacity to distinguish between red and green, M
photoreceptors have photopigments with L opsin in them
tritanopia: incapacity to see any colors but red and green, lack S
photoreceptors entirely
 doesn’t affect visual acuity because there are so few S
photoreceptors
color-opponent neurons: neurons can have receptive fields that are red
inhibitory green excitatory or vice versa, configured in the center-surround
style
at the level of the striate cortex, cells respond to specific kinds of features,
like orientation or shape, rather than simple spots of light
lateral inhibition: the inhibiting effect of one retinal ganglion cell firing on its
neighboring ganglion cells, accounts for the Mach bands illusion
 cell just on the border on the lighter side fires just a little more than
its neighboring cells on the lighter side because it has less lateral
inhibition from the cell on the other side of the border (darker side),
same reason that the cell just on the border on the darker side fires
just a little bit less
simple cells: cells that are excited by a stimulus of one orientation
specifically but inhibited by it being in any other orientation
complex cells: cells that respond preferentially to cells of a certain
orientation but still respond to other orientations to varying degrees, and are
excited by the stimulus being perpendicular to the preferred orientation,
allowing them to also transmit some information about movement
hypercomplex cells: cells that were inhibited at the ends of objects, making
them useful in detecting edges
sine-wave gratings: gratings of lines in a sine-wave fashion
 the pattern of excitatory and inhibitory regions in these kinds of
cells can be graphed as a sine function, and they respond optimally
to stimuli that are sine-wave gratings
 low spatial frequency: most important information about an object,
like its shape and size, processed by the older magnocellular
system
 high spatial frequency: more specific information about an object
like edges and details, processed by the parvocellular system
cytochrome oxidase (CO) blobs: a group of neurons that are highly
metabolically active, revealed by staining their cytochrome oxidase, a
mitochondrial protein
CO blobs in the parvocellular system in the LGN process color information
from cells sensitive to red and green stimuli, CO blobs in the konicellular
system process information from “blue” cells
V2: CO blobs in V1 project to thin stripes (revealed by CO staining) in V2,
which process color and then project to V4, and neurons outside CO blobs in
V1 project to thick and pale stripes in V2, which process information about
movement, orientation, spatial frequency, and retinal disparity
V4: responsible for processing color as well as form, responsible for color
constancy due to its cells’ capacity to inhibit response due to a lot of a
certain wavelength light being present in the surround of the cell’s receptive
field
area TEO (monkey)/V8 (human): important for processing color and form
 in humans, corresponds to parts of the lingual and fusiform gyri
globs: groups of neurons found in V4 and area TEO that respond vigorously
to color and weakly to shapes, neurons outside these globs respond
vigorously to shape and not to color
V5: dedicated to the processing of movement, receives input from the
striate cortex as well as the superior colliculus
area MST: medial superior temporal cortex, dorsal region is important for
the analysis of optic flow

lesions to the dorsal region can leave movement perception intact
except for perception relying on the analysis of optic flow
information
akinetopsia: incapacity to perceive movement resulting from lesions of the
lateral occipital cortex as well as area MST
right medial occipital lobe is responsible for perceiving form from motion
area TE: anterior-most part of the inferior temporal cortex, responsible for
processing information at the most complex level, respond to 3d shapes,
shapes that are partially occluded, moved, or transformed in some way,
respond weakly to simpler stimuli like sine-wave gratings or lines

respond more vigorously to familiar objects than unfamiliar objects,
must play a role in learning
lateral occipital cortex: large portion of the ventral stream that responds to a
wide variety of different specific objects, damage to this area would cause
visual agnosia
dorsal stream: processes movement, spatial orientation and location,
receives input exclusively from the magnocellular system, terminates in the
posterior parietal cortex
ventral stream: processes information about object identification, color,
receives input from the magno-, koni-, and parvocellular streams,
terminates in the inferior temporal cortex
cerebral achromatopsia: loss of color vision due to damage to some part of
the ventral stream
extrastriate body area (EBA): area just posterior to the fusiform face area
and may overlap it slightly, responds to bodies and parts of bodies most
vigorously
parahippocampal place area (PPA): area excited by scenes and backgrounds
but not necessarily their individual features
right fusiform face area is most important for facial recognition
region at the junction of the temporal and parietal lobes, just adjacent to an
area that processes vestibular information, is responsible for compensating
for eye and head movements
intraparietal sulcus: important for visual attention and saccadic movements,
visual control of reaching and grasping, and processing depth perception
from stereopsis

certain region responds only to changes in orientation of objects
that one can grasp
Additional Reading
initial battery of tests allows only discrimination between healthy and braindamaged patients, while a customized battery of tests allows more specific
information on the area of damage and its implications
behaviorally/cognitively, including the cognitive strategy used to arrive at
the response
Wechsler Adult Intelligence Scale (WAIS): intelligence test more suited to
detect brain damage than an IQ test, can suggest right/left hemispheric
damage based on deficits in certain kinds of tasks (e.g. verbal)
 fails to detect memory deficits
sodium amytal test: injection of an anesthetic into one hemisphere of the
brain to test which functions that hemisphere is carrying out alone and which
the other hemisphere is capable of doing
 can be used to determine lateralization of language, dichotic
listening task can also serve this purpose
repetition priming tests: test implicit vs explicit memory, patients can still be
primed to supply certain words despite not consciously recalling having seen
them
phonological language problems: problems interpreting the sounds of
language
Wisconsin Card Sorting Task (WCST): requires the patient to change the
paradigm to which they sort without warning, impossible for patients with
frontal lobe damage, who perseverate in the initial category
reversal learning: rats get two stimuli, have to touch the stimulus that gets
rewarded, and then the stimulus that gets rewarded changes, and they have
to respond to the other stimulus
 like WCST for rats
 rats with frontal lobe damage perseverate as humans do
paired-image subtraction technique: allows the examiner to isolate brain
activity necessary for a specific function by doing two like tasks with the only
difference being the function of interest, subtracting the brain activity allows
the isolation of the brain processes related to the function from other
unrelated processes
open-field test: place the test animal in an empty cage and observe its
anxiety based on the number of times it poops (more=more anxious) and
how often it ventures from the edges
colony-intruder paradigm: introduce an unfamiliar rat to the test animal’s
cage and observe how aggressive it is to it
elevated plus maze: anxiety can be measured based on how much time the
animal spends on the exposed arms of the maze (more time=less anxiety)
conditioned defensive burying: rats bury things that represent negative
stimuli, can be used to study anxiety (less burying=less anxiety)
can also measure the amount of times a male mounts a female, how many
mountings it takes for ejaculation, and how long the male waits to mount
again after ejaculation
lordosis quotient: the proportion of mounts that elicit lordosis, the position
the female takes if she accepts the mounting
conditioned taste aversion: learned aversion to a taste stimulus because of a
negative association afterwards, very readily learned even if the negative
association comes a long time afterwards and only happens once, allows
testing of memory/learning system
radial arm maze: exploits rats’ natural tendencies to explore for food sources
and return only to those locations that result in food, exploration patterns
allows study of memory
Morris water maze: speed with which the rat finds the platform after the first
trial allows study of memory
five-choice reaction time task: measures higher cognitive function
 rat has to detect the light in one of five locations and indicate the
location with a nose poke
 requires them to inhibit impulse to respond before the light goes
on, remember where the light was, plan
delayed response paradigm: requires animal to constantly change which
object to choose, although the rule stays the same (new object), allows tests
of memory
Chapter 7
tympanic membrane: eardrum, vibrates with sound waves
ossicles: the bones of the middle ear (malleus, incus, and stapes) which
vibrate with the tympanic membrane and transfer the vibration to the
cochlea, responsible for the lever effect
oval window: opening to the cochlea, vibrates with the stapes
cochlea is divided into three parts: scala vestibuli, scala tympani, and scala
media (between scala vestibuli and scala tympani)
organ of Corti: sensory receptor in the cochlea, consists of the basilar and
tectorial membranes and hair cells
round window: flexible membrane opening at the other end of the cochlea,
allows the liquid to move back and forth
inner hair cells: transmit information from the vibration of the basilar
membrane to bipolar neurons, which then carry the information to the
auditory cortex in the brain through the cochlear nerve
 action potentials are a result of the hair cells bending towards the
tallest stereocilia
outer hair cells: found on the basilar membrane, important for affecting the
structure of the basilar membrane and thereby amplify the precision of the
information that the inner hair cells receive and transmit, but incapable of
transmitting auditory information themselves
oliveocochlear bundle: axons coming from the superior olive that synapse on
hair cells and inhibit their activity
from the cochlea, some axons synapse on the cochlear nucleus in the
medulla, some travel onto the superior olivary complex in the medulla, then
through the lateral lemniscus to the inferior colliculus, and then the medial
geniculate nucleus and auditory cortex, from where it goes to the cerebellum
and reticular formations
 each medial geniculate nucleus receives bilateral information,
important for preserving tonotopic representation
tonotopic representation on the auditory cortex means that the basal (oval
window) end of the basilar membrane is represented medially on the
auditory cortex, and the apical end is represented laterally
core region: center of the auditory cortex, consists of three regions with
three separate tonotopic maps
belt region: first level of auditory association cortex, receives information
from A1 as well as the medial geniculate nucleus, has seven distinct regions
parabelt region: highest level of auditory association cortex, receives
information from the belt region and the medial geniculate nucleus
dorsal stream of the auditory system: analyzes sound localization,
terminates in the parietal lobe where it overlaps with the visual dorsal
stream and the information is integrated, allowing us to recognize the
collusion of the sight of an object and a sound that it might be making
bird song seems to be analogous to human speech in that there are different
“languages” affected by the origin of the bird, and patterns that are similar
to syllables
ventral stream of the auditory system: analyzes complex sounds, terminates
in the parabelt region
 responds to recognizable but not unrecognizable complex sounds
possible to have auditory agnosia following damage to one of these streams
in the auditory association cortex
bat’s auditory cortex has areas that are specifically tuned to the frequencies
necessary for echolocation and that are dedicated to localizing sounds of
those frequencies
place coding theory: the theory that the frequency of sounds is transmitted
by different areas of the basilar membrane vibrating for different frequencies

the basal end (closest to the oval window) preferentially responds
to high-frequency sounds, while the apical end preferentially
responds to low-frequency sounds
cochlear implants work by stimulating different parts of the basilar
membrane to induce the perception of different frequencies
rate coding: the method by which sounds whose frequency is lower than the
lowest limit of the basilar membrane’s vibrating capacity are transmitted,
not by the part of the membrane that the stimulate but rather the rate at
which they stimulate it
loudness is communicated by the rate of firing of neurons, except for those
frequencies that are communicated through rate coding, for which loudness
is communicated by the number of neurons that are firing
axons that transmit to the auditory areas of the brain have special lowvoltage potassium channels that produce very short and strong action
potentials, which allow for high temporal resolution, which is important for
preserving the perception of sounds, particularly complex sounds

also synapse of the soma of the postsynaptic neuron, which
decreases the time of communication between neurons
pitch discrimination happens in the superior temporal gyrus, harmony
recognition in the inferior frontal cortex, tempo in the right auditory cortex,
and rhythmic patterns in the left, and timing of rhythms in the cerebellum
and basal ganglia
three somatosensory systems
 exteroceptive system: senses external stimuli applied to the skin
o cutaneous senses: skin senses
 proprioceptive system: monitors limb placement and posture
 interoceptive system: senses internal state
encapsulated receptors: receptors that have protective capsules around the
nerve endings, Pacinian, Meissner, and Ruffini all have this
 Pacinian: the capsule serves as a mechanical filter, aiding in the
detection and transmission of vibrational stimuli, generally found
deeper in both hairy and hairless skin
 Meissner: the capsule is designed to transmit light touch
 Ruffini: the capsule is designed to transmit steady pressure,
generally found deeper in both hairy and hairless skin
cold sensors are located closer to the skin surface and transmit information
through thinly myelinated fibers while warm sensors are located deeper and
transmit information through unmyelinated C fibers
 temperature (along with pain) is non-localized, transmitted by
information about broad regions
three types of nociceptors
 high-threshold mechanoreceptors with free nerve endings, respond
to intense pressure
 TRPV1 receptors: free nerve endings that respond to extreme heat,
certain kinds of acid, and the active ingredient in chili peppers
 TRPA1 receptors: responds to inflammatory chemicals
pain can reduce the perception of itching
playing a virtual reality game that stimulates the use of an amputated limb
can relieve phantom limb pain
trigeminal nerve: fifth cranial nerve, transmit information from the face and
head
ventral posterior nuclei of the thalamus: relays somatosensory information
to the primary somatosensory cortex
precisely-localized somatosensory information (like fine touch) is transmitted
through the ipsilateral dorsal column to the medulla and medial lemniscus,
then the ventral posterior nucleus in the thalamus to the somatosensory
cortex, while poorly-localized somatosensory information (like pain) crosses
to the contralateral side
primary and secondary somatosensory cortices have many maps of the
body, each map is thought to respond to a different kind of sensory receptor
damage to the somatosensory association cortex can lead to tactile agnosia
apraxia: incapacity to carry out purposeful movements, leads to an
incapacity to explore objects normally and thereby recognize them by touch,
which goes away if the person’s fingers are guided in a normal pattern of
exploration
absence of the perception of pain seems to arise from a recessive gene on
chromosome 2 that codes for a voltage-dependent sodium channel, called
Nax1.7
anterior cingulate cortex and insular cortex seem to be responsible for the
immediate emotional components of pain

long-term emotional components are mediated by the prefrontal
cortex
 changes in activation of the anterior cingulate cortex don’t change
the perception of pain intensity, but only its level of unpleasantness
 reduced ACC activity can lead to higher pain thresholds
electrical stimulation of the periaqueductal grey matter and the medulla
produce analgesia
 opioids stimulate opiate receptors in the PAG
 PAG sends axons to the nucleus raphe magnus in the medulla and
then onto the dorsal horn in the spinal cord
 analgesia can be evolutionarily adaptive to promote adaptive
behaviors (self-defense, paternal instincts, reproduction)
production of endogenous opiates in the ACC and insular cortex that then
produce the same effects, as well as increased activity in the prefrontal
cortex and PAG can be triggered by the administration of a placebo
Chapter 8
movement commands originate in the primary motor cortex, and are
modified by the cerebellum and basal ganglia after, which helps make them
more exact and precise
duration of stimulation of the motor cortex varied the complexity of the
movement, whereas location of the stimulation varied the kind of movement
supplementary motor area: one of the primary inputs to the primary motor
cortex, located medially and just anterior to the primary motor cortex,
important for carrying out sequences of movement by planning the next
movement to come (but not the execution of the actual movement)
 get input from the parietal lobe that indicates that a decision to
move has been made
pre-supplementary motor area: responsible for the production of
spontaneous movements, stimulation produces a sensation of a desire to
move or anticipation that movement is about to occur
arbitrary information: information the indirectly guides movement (reach to
the left when a red light flashes)
nonarbitrary information: information that directly guides movement (reach
for an object located to the left)
premotor cortex: another primary input to the primary motor cortex, located
laterally and just anterior to the primary motor cortex, important for
learning arbitrary associations between stimuli and movement
somatosensory cortex also sends information to the primary motor cortex
from corresponding body parts/areas
lateral group: descending system from the motor cortex through the spinal
cord that controls movements where that of one side differs from the other
ventromedial group: descending system that controls more automatic
movements in coordinated limb movements
temporal and parietal lobe provide motor cortex and motor association
cortex with information about what’s happening and where that’s necessary
to co-ordinate movement
mirror neurons are located in the ventral premotor cortex (F5), which is
connected with the inferior parietal lobule, which also has mirror neurons
 evidence that mirror neurons respond not only to an action, but to
its intention
 mirror neurons can be activated by the sound associated with an
action

important for imitating movements, as well as for understanding
other peoples’ intentions and subsequent actions
parietal reach region: area of the medial posterior parietal cortex that plays
an integral role in coordinating reaching movements
anterior intraparietal sulcus: coordinates the mechanism of grasping an
object, also involved in recognizing grasping movements
apraxia: incapacity to produce movement in response to verbal instruction
due to damage to the left frontal or parietal lobes
limb apraxia: movement of the wrong part of the limb, incorrect movement,
or incorrect sequence of movement, incapacity to pantomime acts but can
usually do them if the relevant object is there
 left parietal damage causes limb apraxia in both hands, thought to
be because the left parietal lobe is more involved with one’s own
body, while the right parietal lobe is more involved with
extrapersonal space
constructional apraxia: incapacity to assemble objects correctly in 3d or in
pictures, as well as a severe difficulty with maps or anything requiring an
understanding of spatial relationships, due to damage to the right parietal
lobe
basal ganglia receive input especially from the primary motor and
somatosensory cortices and the substantia nigra, and send output mostly to
the primary motor cortex, SMA, the premotor cortex, and the motor nuclei in
the brain stem
 made up of the caudate nucleus, the putamen, and the globus
pallidus
o caudate nucleus and putamen receive input from the frontal,
parietal, and temporal lobes, and then transmit it to the
globus pallidus
o globus pallidus sends information to the motor cortex through
the ventral anterior and ventrolateral nuclei in the thalamus
direct pathway: pathway through the internal globus pallidus that originates
in the caudate nucleus and putamen, which inhibit the internal globus
pallidus when excited, which then sends inhibitory axons to the thalamus,
which sends excitatory signals to the motor cortex, increases movement
indirect pathway: pathway through the external globus pallidus that
originates in the caudate nucleus and putamen, which inhibit the external
globus pallidus when excited, which then sends inhibitory axons to the
subthalamic nucleus, which then excites the internal globus pallidus, which
then sends excitatory axons to the thalamus, which sends inhibitory signals
to the motor cortex, reduces movement
Parkinson’s disease: characterized by slowness to initiate movement
(hypokinetic symptoms) and movement being uncoordinated once initiated,
probably results from a lack of inhibitory output from the direct and indirect
pathways due to a decrease in dopamine levels in the substantia nigra
Huntington’s disease: characterized by spontaneous uncontrolled
movements (hyperkinetic symptoms, also symptomatic of Tourettes
syndrome), caused by a degradation of the caudate nucleus and putamen,
especially their GABAergic and acetycholinergic neurons, causing decreased
activity of the indirect pathway
 caused by a dominant gene on chromosome 4 that codes for
increased glutamine
flocculonodular lobe: involved in reflexes, located on the caudal end of the
cerebellum
vermis: located on the midline, gets auditory, visual, and vestibular
information and outputs to the fastigial nucleus, which sends outputs to the
vestibular and motor systems
intermediate zone: area in the cerebellum that controls arm and leg
movements through projections to the interposed nuclei and then onto the
red nucleus
lateral zone: area in the cerebellum that controls independent limb
movements, receives information about planned movement from the motor
cortex through the pontine nucleus, and from the somatosensory cortex,
outputs to the dentate nucleus, which is important for the integration of
successive movements and therefore their planning
cerebellum is especially important for the timing of rapid, precisely aimed
movements
reticular formation is important for posture as well as locomotion
Chapter 9
alpha activity: regular medium frequency brain waves that occur when we’re
relaxed, mostly when our eyes are closed
beta activity: irregular low-amplitude brain waves that occur when we’re
actively processing information
 shows desynchronized activity, which occurs when several different
neural units are processing simultaneously
theta activity: more synchronized neural firing characteristic of stage 1 sleep
and the transition between sleep and wakefulness, decreased frequency and
increased amplitude, muscles relax
stage 2 sleep: characterized by mostly irregular activity, but with K
complexes and sleep spindles, if wake up after stage 2 sleep, have the
impression of not having slept

sleep spindles: short bursts of waves that occur throughout stages
1 to 4, seem to be important for better cognitive functioning after
naps as well as preventing premature waking
 K complexes: sudden, sharp waveforms that occur exclusively in
stage 2 and can be triggered by noise, seem to serve as an
inhibitory mechanism preventing the sleeper from waking
delta activity: high-amplitude brain activity that occurs in stages 3 and 4,
collectively known as slow-wave sleep
 activity is characterized by slow oscillation of about 1 Hz, down
oscillations of the down state indicate inhibition and inactivity of
neurons, up periods of the up state show neurons briefly firing at a
high rate
 other activity in slow-wave sleep are synchronized with these
oscillations
 stages 3 and 4 are characterized by decrease in cerebral
metabolism and thought to be important for memory consolidation
REM sleep: sleep stage characterized by paralysis and rapid eye movements
as well as increased cerebral metabolism and desynchronized brain activity,
can only be awakened by loud noises or meaningful stimuli, and dreaming,
periods of REM and non-REM sleep alternate, with periods of REM becoming
longer as sleep lasts longer
 eye movements seem to correspond to what the person’s eye
movements actually would have been had they been watching what
they were dreaming about, as does brain activity
 REM sleep seems to be necessary for feeling well-rested (but won’t
die if we’re deprived of it, as with slow-wave sleep), sleep



medication that only induced stages 1-4 of sleep resulted in people
experiencing a sleep hangover and not feeling like they’d actually
slept
also important for structural changes that are necessary for brain
development (early brain development and learning later in life)
vaginal secretions and penile erections increase even if the content
of the dream is non-sexual
blood flow to the primary visual and prefrontal cortices is low during
dreaming, but high blood flow to the visual association cortices,
producing hallucinations when we dream, low blood flow to the
prefrontal cortex probably accounts for the lack of temporally
organization of dreams
o PGO waves: bursts of activity just before and during REM
from the pons to the LGN to the visual cortex, seem to be
related to the onset of dreams
all mammals and birds engage in REM sleep, reptiles and amphibians
undergo a period of inactivity that’s similar to mammalian sleep, but don’t
experience REM with muscular inactivation
in dolphins, one hemisphere sleeps at a time, which allows the detection of
predators (in which case both hemispheres wake up) and the coordination of
periodic resurfacing to get oxygen
variation in sleep times between animals seems to be correlated to whether
they’re predators or prey (prey sleep less, need to be more alert)
sleep apnea: condition where the person stops breathing while they’re
sleeping, causing build-up of CO2 in the blood, stimulating chemoreceptors
that cause the person to wake up and breathe, restoring oxygen levels
sleep attack: overwhelming urge to sleep during boring situations, sleep
usually lasts about 5 minutes, symptom of narcolepsy, can be treated by
stimulants
cataplexy: person experiences the paralysis of REM sleep while fully
conscious, usually brought on by strong emotions or sudden physical
exertions, symptom of narcolepsy, can be treated by drugs that facilitate
serotonergic and noradrenergic activity
sleep paralysis: inability to move just before or after sleeping
hypnagogic hallucinations: dreams while awake
narcopleptic patients will wake up often in the middle of the night and skip
the first stages of sleep to go directly into REM
 seems to be caused by a gene mutation, causing a deficit of orexin
receptors, either because the immune system attacks and destroys
them, or because they’re not manufactured in the first place
o can also be caused later by stroke or other brain damage to
orexin/orexin receptor production
REM sleep behavior disorder: disorder in which people aren’t paralyzed
during REM sleep and therefore act out what they’re dreaming about,
thought to be a genetic disorder, treated by benzodiazepines
sleep-related eating disorder: kind of sleepwalking disorder in which people
eat during slow-wave sleep, can be genetically determined or caused by
certain insomnia medication, can be treated with dopaminergic agonists or
anti-anxiety drugs
insomnia can be caused by drugs, hormonal shifts, psychological problems
(e.g. stress, anxiety), changes in circadian rhythm, or abuse of sleeping
medication
sleep seems to be important for maintaining cognitive function and therefore
allowing the brain to rest, not so much the body
oxidative stress: stress caused by the high metabolic rate of the brain
causing a large number of free radicals mitigated by slow-wave sleep,
especially stage 4, which is characterized by extremely low metabolic activity
in the brain and thereby allows the brain to repair the damage wreaked
during the oxidative stress
 slow-wave sleep seems to be important to repair damage to regions
that were particularly active during the day
 free radical: lone oxygen atom (electron) that’s highly reactive and
will destroy everything in its path to bind with something to form a
molecule
fatal familial insomnia: hereditary disorder causing severe sleep disturbances
and eventually death as a result
rebound phenomenon: tendency of people to spend a greater percentage of
sleep in REM sleep and slow-wave sleep (rather than stages 1 and 2) after
sleep deprivation, indicating that REM is perhaps the most important stage
of sleep

also a relatively high percentage of REM sleep during periods of
brain development
experiment with rats where both rats were forced to walk on a motor board
when the EEG of one showed that it was falling asleep, effectively forcing
both to be equally physically active while only depriving one of sleep, sleepdeprived rat became very unhealthy and eventually died
REM sleep seems to be particularly important for consolidation of nondeclarative memories, while slow-wave sleep is important for the
consolidation of declarative memories
modulation of the sleep cycle: the longer we’re awake, the lower the
glycogen levels are in our brain, causing the extracellular adenosine levels to
rise, which has an overall inhibitory effect on neural activity
 sleep allows astrocytes to replenish their stocks of glycogen
 caffeine blocks adenosine receptors, allowing us to stay awake for
longer because the adenosine can’t have the same inhibitory effect
acetylcholinergic neurons located in the pons and basal forebrain are integral
to stimulation, produce activation and desynchronous activity when
stimulated
 in the hippocampus and neocortex, ACh levels were high during
wakefulness and REM sleep, but low during slow-wave sleep
locus coeruleus: noradrenergic system located in the pons that plays a role
in wakefulness and vigilance, high firing during wakefulness, low during
slow-wave sleep, and practically nothing during REM sleep
raphe nuclei: located in the reticular formation, house almost all the
serotonergic neurons, thought to be necessary for suppressing sensory
processing to promote the continuation of already existing activity, promotes
continuous movement
 serotonergic neurons fire decreasingly in slow-wave sleep and then
increases greatly during REM
tuberomammillary nucleus: located in the hypothalamus just next to the
mammillary bodies, houses histaminergic neurons, which are thought to be
relevant for arousal, connections to the acetylcholinergic neurons in the
basal forebrain increase ACh release in the cortex
lateral hypothalamus: has orexinergic neurons, important for arousal and for
stabilizing the flip between sleep and wakefulness, maintaining us in one
state for a longer period of time
ventrolateral preoptic area in the hypothalamus is responsible for
mechanisms of falling asleep and the sensation of drowsiness
 houses sleep neurons, which secrete GABA and send inhibitory
outputs to the lateral hypothalamus, tuberomammillary nucleus,
dorsal pons, raphe nuclei, and locus coeruleus
 gets input from the tuberomammillary nucleus, raphe nuclei and
locus coeruleus, which inhibit it and therefore promote wakefulness
 which part of the sleep “flip-flop” we’re in depends on which region
is inhibiting the other more
sublaterodorsal nucleus: houses acetylcholingergic REM-ON neurons,
stimulation induces REM sleep and inhibition disrupts it, mutually inhibits
REM-OFF neurons, meaning only one area can be active at a time
 neurons responsible for muscular paralysis are located just ventral
to this area, and inhibit motor neurons in the spinal cord, damage
to this area causes REM sleep behavior disorder
 pedunculopontine nucleus and laterodorsal tegmental nucleus are in
the peribrachial area and house acetylcholinergic neurons whose
activity promotes REM sleep
ventrolateral periaqueductal grey matter: houses REM-OFF neurons,
stimulation suppresses REM sleep, while inhibition greatly increases it,
receives excitatory input from the lateral hypothalamus during wakefulness
(as well as the locus coeruleus and the raphe nuclei), when we begin to
sleep, the activity of these areas decreases and therefore their output
decreases, until the inhibitory output of the REM-OFF neurons to the REMON neuron decreases sufficiently for the flip to occur
 reason why the lack of orexin receptors causes cataplexy and why
they’re so important for stabilizing the flip-flop cycle, seems that
they provide an inhibitory influence from the hypothalamus on the
amygdala, without them, increased amygdala activity can flip the
cycle into REM-ON
orexinergic neurons fire at the highest rate during wakefulness and active
exploration, and at the lowest rate during slow-wave and REM sleep
 necessary for maintaining muscle tone even during a high level of
arousal, lack of orexin receptors in people with narcolepsy explains
the paralysis
REM sleep disorders occur when muscular paralysis doesn’t, people act out
their dreams
sleep walking isn’t a REM sleep disorder, not acting out dreams, occurs
during slow-wave sleep and person is a low-conscious version of their
conscious self
 other slow-wave sleep disorders: bedwetting, night terrors
suprachiasmatic nucleus: responsible for maintaining the circadian rhythm,
gets input from melanopsin photoreceptors in the retina about whether it’s
day or night
 projects to the ventrolateral preoptic area and the lateral


hypothalamus, promoting sleep or wakefulness, respectively
“ticks” through neurons where the production in one loop eventually
inhibits the production in a second, causing the cycle to start over,
corresponds to a set cycle length
also modulates bodily cycles that correspond to seasons along with
the pineal gland
o pineal gland produces melatonin, which acts on various
structures to control behavior and physiological processes
that vary with the seasons
Chapter 10
estrous cycle: reproductive cycles of mammals other than humans
ovarian follicles: epithelial cells that form around the ovum, growth
stimulated by hormones secreted by the pituitary gland, if two are produced,
woman will have twins, secrete estradiol as they grow which eventually
triggers ovulation
ovulation: the rupture of the ovarian follicle, turning it into a corpus luteum,
which produces estradiol and progesterone, which maintains the lining of the
uterus and prevents another follicle from being produced
 if the ovum is fertilized, it will start to divide and attach to the
uterine wall; if it isn’t fertilized, the corpus luteum will stop
producing progesterone and estradiol and menstruation will start
sexual activity in male rates is moderated by testosterone, which is
produced by the testes, castrated rats will only show sexual behavior if given
testosterone injections as adults
if male rodents are presented with a new female after having been
exhausted by sex with one female, they’re capable of having sex with the
new female with renewed vigor
oxytocin: hormone released by the posterior pituitary gland during breast
feeding and orgasm, important for establishing pair bonding
lordosis: position that the mammalian female takes in response to mounting
by the male if she’s receptive, facilitates intercourse
 increases in estradiol and then progesterone are necessary for
sexual receptivity, ovarectomized females are not sexually receptive
o estradiol is necessary for progesterone to be effective
o hormones also increase attractiveness of female and her
eagerness to mate, as well as her ability to mate
if animals aren’t exposed to androgens shortly after birth, during the critical
period, they will exhibit female sexual behavior as adults
if they are exposed to androgens during the critical period, animal doesn’t
display female sexual behavior in adulthood (behavioral defeminization) and
will display male sexual behavior (behavioral masculinization), if exposed to
female sex hormones in adulthood, will show no sexual behavior
only time when hormone injections in adulthood can affect rodent sexual
behavior is when they weren’t exposed to male or female sex hormones
during the critical period (usually because of being ovarectomized/castrated)
or if the exposure to the hormones is extended, like with sex change
operations
 rats exposed to no hormones during the critical period and
testosterone later show no sexual behavior
Lee-Boot effect: if female mice are housed together away from males, their
estrous cycles will slow and eventually stop
Whitten effect: the reversal of the Lee-Boot effect if the females are exposed
to male urine, also causes the females’ cycles to become synchronized
Vandenberg effect: acceleration of the onset of puberty in a female after
being exposed to male odor
Bruce effect: tendency of a pregnant female’s pregnancy to fail if she’s
exposed to the urine of a male other than the father, evolutionarily adaptive
because then the male is probably dominant and can impregnate her
himself, and the female’s offspring will be that of the dominant male
vomeronasal organ: located in the nasal passage, receptors sensitive to
chemicals that serve as pheromones (specifically when they’re in urine or
other substances), projects to the accessory olfactory bulb, and then onto
the medial nucleus of the amygdala to the ventromedial hypothalamic nuclei,
can allow detection of gender and identity as well as estrous condition (and
therefore sexual receptivity)
 its destruction disrupts the Lee-Boot, Whitten, Vandenberg, and
Bruce effects
 primary olfactory system is responsible for initiating the original
investigation of another animal, also capable of detecting some
pheromones
 destruction of the medial amygdala abolishes male rodent sexual
behavior, important for the mediation of pheromone information
women exposed to men’s sweat advanced their next menstrual cycle, and
were more relaxed
 exposure to an androgenic chemical increased positive mood in
women, and decreased positive mood in men
men reported that t-shirts worn by women in the fertile stage of their cycle
smelled sexier than those worn by women in their infertile stage
in humans, chemical signals seem to be detected by the primary olfactory
system and not by a vomeronasal organ
study of lesbian couples suggested that ovarian hormones cause an increase
in sexual interest in the middle of the women’s cycles
 women are most likely to initiate during the peak of their cycles,
when estradiol levels are the highest
 men are always equally likely to initiate
 androgens in conjunction with estradiol seem to amplify estradiol’s
effects on sexual interest
the most sexually dominant monkeys would continue to copulate for weeks
after their testosterone production had been suppressed, whereas the
copulation of lower-ranking monkeys would cease until testosterone
secretion re-attained normal levels
prenatal exposure to androgens seems to be the most likely biological cause
of homosexuality
congenital adrenal hyperplasia: disorder in which the adrenal glands secrete
abnormally high amounts of androgens, causing prenatal masculinization

has little to no effect on boys, but girls are born with an enlarged
clitoris and partly fused labia, and are also more likely to be sexually
attracted to women, as well as to draw pictures with more male
motifs and play with traditionally male toys
exposure to androgens prenatally seems to have a masculinizing effect that
strongly encourages male sexual identification, even if the child is brought
up as a female
males with androgen insensitivity syndrome show no sexual behavior as
adults because they’re de-feminized and de-masculinized, if given female
sex hormones and remove testes, display normal female sex behavior as
adults
brain sexual dimorphism seems to be the result of prenatal exposure to
androgens
brain activity in response to exposure to two chemicals that seem to be
human pheromones, AND and EST, was similar in homosexual males and
heterosexual females
 people sexually attracted to males showed stimulation in the
preoptic area and ventromedial hypothalamus in response to AND,
while people sexually attracted to females showed stimulation in the
paraventricular and dorsomedial nuclei in the hypothalamus in
response to EST
bed nucleus of the stria terminalis: nucleus whose size seems to be
correlated to sexual identity, smaller in females than males and equal size in
male-to-female transsexuals as in females (same results with female-tomale transsexuals)
 doesn’t necessarily show causation, could be a third factor like
exposure to prenatal hormones that caused both
exposure to stress in pregnant mothers suppresses prenatal androgen
production for male fetuses
 these male fetuses were less likely to show male sexual behavior
and more likely to show female play behavior and female sexual
behavior if exposed to estradiol and progesterone
evidence that some mothers who have had several male children become
sensitized to proteins that only male fetuses possess, which may affect the
prenatal development of subsequent male fetuses, which would explain the
increase in likelihood of these subsequent males of being gay
identical twin studies have shown that male homosexuality is at least
somewhat heritable
 evolutionary explanation: female maternal relatives of male
homosexuals tend to be much more fertile, suggesting that a gene
on the X chromosome has an effect on male homosexuality and
female fertility
ejaculation stimulates neurons in the spinal cord that project to the posterior
intralaminar thalamus
medial amygdal lesions abolished sexual behavior in male rodents
medial preoptic area: located just next to the hypothalamus, important for
male sexual behavior as well as other sexually dimorphic behaviors, like
maternal behaviors
 act of copulation increases activity here in males, stimulation
increased rate of ejaculation
 receives input from the VNO and olfactory system through the
medial amygdala and BNST as well as genital somatosensory
information
 castrated males’ sexual behavior can be re-instated by stimulus of
the MPA

lesions disrupt nest building and taking care of pups in females, but
not sexual behavior
 also seems to play somewhat of a role in paternal behavior
sexually dimorphic nucleus: located in the preoptic area, much larger in
males, size is determined by exposure to prenatal androgens
periaqueductal grey matter: connects the MPA to the spinal cord, important
for initiation of lordosis in females through the pathway from the VMH to the
PAG to the nucleus paragigantocellularis to the motor neurons in the spinal
cord
nucleus paragigantocellularis: in the medulla, inhibits spinal cord reflexes,
MPA inhibits this thereby allowing ejaculation to occur
 activity is agonized by SSRIs, suppressing ejaculation
ventromedial nucleus of the hypothalamus: important for female sexual
behavior
vasopressin seems to play a role in monogamy, specifically levels in the
ventral forebrain
oxytocin has been shown to increase relaxation and trust and reduce anxiety
female rats lick the genital area of their young, thereby inducing excretion
and also drinking the urine, allowing them to regain about 2/3 of the water
they lose through lactating
passage of the pups through the mother’s birth canal seems to stimulate
maternal behavior
 progesterone, estradiol, and prolactin in a specific sequence in the
MPA and timing seem to be responsible for the initiation of maternal
behavior and suppression of the natural aversion to the smell of
pups
o medial amygdala seems to be responsible for transmitting the
information about the pups’ smell
dopaminergic system of the ventral tegmental area to nucleus accumbens is
important for motivation and reinforcement, and is activated in maternal
behaviors
 when maternal behaviors are activated, other stimuli that normally
activate this circuit, like cocaine, have less of an effect
Chapter 11
behavior component of emotion: muscular movements that are responses to
a particular situation
autonomic component of emotion: facilitate response behaviors, allowing
quick and vigorous response if necessary
hormonal component of emotion: reinforce autonomic response system
lateral nucleus: subdivision of the amygdala, receives information especially
from the ventromedial prefrontal cortex, the thalamus, and hippocampal
formation, and sends it especially to the basal nucleus and ventral striatum
and the prefrontal cortex via the dorsomedial nucleus of the thalamus
basal nucleus: subdivision of the amygdala, receives information from the
lateral nucleus, and sends information to the central nucleus along with the
lateral nucleus
central nucleus: subdivision of the amygdala that receives information from
the basal and lateral nuclei of the amygdala and projects to the
hypothalamus, midbrain, pons, and medulla, most important part of the
brain for emotional responses to aversive stimuli

control autonomic and endocrine responses that result in the effects
of long-term stress, its lesioning eliminates standard somatic
responses to stress (e.g. ulcers)
 site of learning, along with the lateral nucleus
mammillary bodies: on the ventral surface of the brain, attached to the
fornix
fornix: carries information from the hippocampus to the septum and
mammillary bodies
septum: on the midline of the brain, attached to the corpus callosum and
fornix, connected to the amygdala and hippocampus
ventromedial prefrontal cortex: communicates with many areas of the brain
including other parts of the prefrontal cortex, and is responsible for the
extinction aspect of learning and important for controlling the expression of
emotion, inputs generally provide it with information about what’s going on
and outputs allow it to regulate behavioral and physiological responses to
environmental events
 extinguished responses aren’t forgotten, ventromedial prefrontal
cortex simply suppresses the expression of the response
 people with damage here have trouble distinguishing between


important and trivial decisions, and in applying proper social
behavior to real-life situations, tend to make utilitarian moral
judgments
making moral judgments activated the ventromedial prefrontal
cortex, along with other areas associated with emotion and
emotional processing
destroyed in Phineas Gage, no capacity to understand
consequences of behavior, make decisions based on short-term
rather than long-term gains (e.g. Iowa Gambling Task)
o patients with ventral prefrontal damage only showed
physiological changes associated with stress after learning
that they’d lost money, not before picking from the “bad”
deck, as normal patients did, and those with amygdala
damage never showed any physiological changes, damage
meant they couldn’t benefit from subconscious systems
discouraging choice from the “bad” deck

psychopaths show abnormal activation in this area and in its
connections to the amygdala
when moral judgments cause a conflict between emotional and rational
factors, the anterior cingulate cortex becomes activated, which stimulates
the dorsolateral prefrontal cortex, which mediates the two factors
amygdala seems to be necessary for the experience of the emotion of fear
 responsible for the augmentation of startle response when negative
emotion is elicited, likelihood that the event provoking the startle
response necessitates action is greater if negative emotion is
present



responsible for increased memory retention for things associated
with emotion (effect goes away if person’s amygdala is lesioned)
when an animal is being attacked, amygdala activity is high, but
when an animal is attacking, amygdala activity tends to be low
o attack can be elicited by stimulation of the periaqueductal
grey matter, which is affected by excitatory and inhibitory
connections with the hypothalamus and amygdala
psychopaths don’t show conditioned fear response that normals do,
which seems to be dependent on the amygdala
serotinergic neurons in the forebrain seem to play a central role in inhibiting
risky behaviors, including aggression, and mediating impulse control
 people with a genetic mutation affecting the serotonin transporter,
which determines how much serotonin remains in the terminal
button after it’s released, show higher amygdala activation when
looking at faces expressing fear or anger
increased amygdala activity is correlated with increased display of negative
emotions, and decreased prefrontal activity is correlated with decreased
inhibition of the display of and control over these emotions
 increased serotonin release increases prefrontal activity
increased early exposure to androgens in males sensitizes the neural circuits
associated with aggression and thereby decreases the exposure to
androgens necessary later in life to stimulate aggression
 testosterone facilitates aggression in females as well as in males
 female mice that were closer to males in utero were exposed to
more androgens prenatally and had correspondingly higher levels of
testosterone in their blood and were correspondingly more likely to
be aggressive as adults
 girls show increased aggressiveness if they shared a uterus with a
brother, but not increased testosterone levels
anti-androgen drugs have been shown to have an effect, but only on sexrelated aggression (and sex drive)
 possible that androgens play a role in drive for dominance, which
often dovetails with aggression, study showed that specifically men
of lower socioeconomic status with higher testosterone levels
displayed more aggression
o people who win at a game have a higher level of testosterone
after winning
in dominant monkeys, alcohol increased aggressive behavior if combined
with an injection of testosterone
right hemisphere seems to be more relevant in comprehension of emotion
 comprehension of emotion through words activated the prefrontal
cortex bilaterally, but the left preferentially, comprehension of
emotion through tone of voice activated exclusively the right
prefrontal cortex
lesioning of amygdala eliminates capacity to learn fear responses in rats,
although it’s impossible to know if the rat experiences fear
 monkeys with lesioned amygdalas showed no delay in reaching over
fearful stimuli to retrieve food
facial expressions are universal across cultures, as Darwin theorized,
because being able to communicate emotional responses is highly
evolutionarily adaptive
amygdala seems to be necessary for visual recognition of facial expressions
of emotion, but not for emotional comprehension through tone of voice

visual recognition seems to rely on input from the magnocellular
system, through the superior colliculus and the pulvinar, which
means that this system can recognize this information using lowbut not high-frequency visual information
o contrast with the fusiform face area, which relies on the
parvocellular system and therefore can recognize faces using
high- but not low-frequency visual information




affective blindsight: capacity to recognize facial expressions of
emotion despite damage to the visual cortex causing blindness
body language information facilitates recognition of facial
expression of emotion
amygdala seems to direct visual exploration of the face to the eyes
and area surrounding them, facilitating recognition of emotion,
pictures of “fearful” eyes alone is enough to cactivate the amygdala
amygdala damage may mean that the person doesn’t recognize
that the comprehension of emotional expressions is valuable
information and therefore doesn’t engage in behavior to discover it
superior temporal sulcus in monkeys is important for recognizing the
direction of another creature’s gaze
 connections between the superior temporal sulcus and parietal
cortex, allows direction of attention to follow others’ gaze
damage to the right somatosensory cortex severely inhibits capacity to
recognize facial expressions of emotion, presumably because it renders us
incapable of mentally (or physically) mimicking the facial expression
same system of mirror neurons can be activated by a visual or auditory
stimulus expressing the same emotion
insular cortex and basal ganglia are important for the recognition of the
expression of disgust
 respond to expression of disgust or judged expression of disgust,
even if actual expression is neutral
volitional facial paresis: caused by damage to the face region of the primary
motor cortex or its connections to motor neurons that control facial muscles,
incapacity to express facial expressions voluntarily, but can express genuine
emotion involuntarily
emotional facial paresis: caused by damage to the insular region of the
prefrontal cortex, white matter in the frontal lobe, or thalamus, capable of
moving facial muscles voluntarily but incapable of expressing emotion with
facial muscles
anterior cingulate cortex seems to be responsible for the muscular
movements involved in laughter, right ventromedial prefrontal cortex is
responsible for comprehension and appreciation of humor
left halves of peoples’ faces tend to be more expressive and show emotional
expression sooner than the right, suggesting that the right hemisphere is
more expressive
patient with amygdala lesion was incapable of recognizing facial expressions
of fear, despite retaining the capacity to generate fear expression in
response to fearful stimuli
principle of antithesis: comes from Darwinian theory, effective emotional
expressions must have opposite emotions that are expressed by
correspondingly opposite signals
common sense view of emotion: a feeling of fear leads to the physiological
response to the stimulus that caused that fear
Papez circuit: circuit from cingulate cortex to hippocampus to hypothalamus
to anterior thalamus to cingulate cortex, behavior emerges from
hypothalamic activity while subjective experience of emotion arises from
cingulate cortex activity
James-Lange theory of emotion: stimuli induce physiological responses,
which then produce our experience of a certain emotion through sensory
feedback
 Cannon’s criticism: cutting fibers that provide sensory feedback


didn’t cause a change in emotional behavior in animals, turns out to
be irrelevant because the James-Lange theory was about the
experience of emotion, which is impossible to study in animals, who
can’t self-report on their experience of emotion
another criticism: internal organs are insensitive and don’t respond
quickly enough to stimuli to account for our instantaneous
experience of emotional feeling
the higher up a person has a spinal cord injury, the less intense
their feeling of emotion, despite their emotional behavior remaining
constant
 making different facial expressions produced physiological changes
corresponding with the emotions being expressed
o possible that this has been established through classical
conditioning based on experience, or that it’s innate
Kulver-Bucy syndrome: bilateral bisection of amygdala and surrounding area
caused reduction in fear reactions, as well was hypersexuality,
hyperaggressiveness, hypermetamorphosis (increased inspection of
everything despite lack of recognition of familiar objects), and highly oral
level of activation of frontal mirror neurons in 10-year-olds watching facial
expressions was positively correlated with measures of their empathetic
behavior and interpersonal skills
periaqueductal grey matter in cats is responsible for both predatory and
defensive behavior, has connections with the hypothalamus and amygdala
that affect overall expression of an emotional response
Chapter 12
different animals have different eating patterns that correspond to varying
lifestyles
 snakes and crocodiles, which need less energy, will eat huge
amounts and then not eat for a period of time
 bears will eat as much and as often as they can, because their food
supply is season-dependent
o pandas will avoid activity to save energy if necessary
 birds will eat only when they need it, and store very little, which is
dangerous if their food supply dries up

monkeys and humans will eat more than they need for energy at
the moment and then store the excess energy for later
glycogen: carbohydrate that makes up the short-term reservoir in the liver
and muscles
 liver is stimulated to convert glucose into glycogen and store it by
the presence of insulin, released by the pancreas when the level of
glucose in the blood is high
 liver is stimulated to convert glycogen into glucose by the presence
of glucagon, released by the pancreas when the level of glucose in
the blood is low
 short-term reservoir store of energy is reserved for the central
nervous system, which gets its energy from there until it’s
depleted, at which point it begins drawing on the long-term
reservoir, or until we eat again
prolonged high or low insulin levels both increase eating

prolonged high insulin levels mean that glucose will continue to be
moved into cells, causing the blood glucose level to drop and
causing hunger shortly after eating
 prolonged low insulin levels mean that blood glucose levels will stay
high, but very little will enter cells, causing the cells to effectively
starve as the glucose is excreted, increasing eating and weight loss
triglycerides: glycerol with three fatty acids that make up adipose tissue that
is our long-term reservoir
 adipose tissue consists of cells that can absorb nutrients from the
blood and convert them into triglycerides
o cells are capable of expanding in size to store more
triglycerides, obese people have larger adipose cells
o breaks triglycerides down into glycerol and fatty acids when
the digestive system is empty, provide energy to everywhere
in the body but the brain, which can only process glucose
o glucose can only enter cells in the rest of the body through
glucose transporters that are only active when insulin is
present, glucose transporters in the brain are functional with
or without the presence of insulin
fasting phase: part of the eating cycle when nutrients aren’t available from
the digestive system, so cells derive their fuel from the short- and long-term
reservoirs
absorptive phase: part of the eating cycle when cells can absorb nutrients
directly from the digestive system, pancreas secretes insulin which allows all
the cells to use glucose and stimulates the liver to build up its store, amino
acids are used as building blocks and converted to adipose tissue, as are fats
and extra glucose
the tastes and corresponding diets of mammals change over the course of a
lifetime (e.g. lactose intolerance in most mammals after infancy)
 the content of the mother’s milk changes over the course of the
infant growing up, providing different nutrients that are important
at different points in development
herbivores and omnivores rely on others to learn what provides adequate
nutrition, facilitates group social structure
environmental signals (e.g. cooking, smelling food) can induce eating, even
without the biological hunger signals
ghrelin: hormone released by the digestive system (especially the stomach)
when the digestive system is empty and we should be seeking out food, not
affected by the presence of nutrients in the blood
 involved in the release of growth hormone
 levels increase with fasting and decrease directly after a meal
 stimulates feelings of hunger
glucoprivation: stimulation of eating by depriving cells of glucose through
hypoglycemia (fall in glucose levels in the blood) or the infusion of 2-DG,
which competes with glucose to bind to glucose transporters but doesn’t
actually provide the cells with glucose
lipoprivation: stimulation of eating by depriving cells of lipids by depriving
them of the ability to metabolize fatty acids
receptors in the liver that monitor lipid and glucose levels in the blood and
sends hunger signals to the brain through the vagus nerve when these levels
drop too low
receptors in the dorsomedial and ventrolateral medulla monitor glucose
levels but not lipid levels, because the brain can’t process lipids as fuel
process of eating and swallowing food contribute to a feeling of satiety
rats have receptors in their stomachs and intestines that measure both the
volume of food and its nutritive quality
cholecystokinin (CKK): hormone secreted by the duodenum in response to
the presence of fats whose presence inhibits gastric contractions and thereby
the stomach from giving the duodenum more food, inhibits eating
 acts on receptors at the junction of the stomach and duodenum,
signals are then transmitted to the brain through the vagus nerve
PYY: chemical released by the gastrointestinal tract in proportion to the
number of calories consumed, inhibits appetite
liver produces a signal to the brain that inhibits appetite when it receives
nutrients
insulin receptors in the hypothalamus also contribute to satiety signals,
insulin is actively transported across the blood-brain barrier
long-term satiety signals can affect the sensitivity to short-term satiety
signals
 rats that are force fed or starved will alter the amount that they eat
 but, in general, long-term satiety signals don’t regulate weight
 come from monitoring of fat cells through leptin levels
leptin: peptide secreted by well-nourished fat cells, satiety signal
 ob rats: rats that are obese because of a mutation of the OB gene
that’s responsible for leptin production
 fructose: in most fast foods, reduces the level of leptin and
therefore stimulates hunger shortly after its consumption
brain stem contains neural circuits that respond to certain hunger and
satiety signals, and plays some role in food intake
area postrema and nucleus of the solitary tract contain glucose receptors,
hunger increases their activity and lesions there abolish glucoprivic and
lipoprivic eating
lesions of the lateral hypothalamus abolish eating and drinking, stimulation
produces both
 connections to the NST which affect taste perception, to the parts of
the cortex and spinal cord controlling, ingestion, swallowing, and
digestive secretions, and to the pituitary gland increasing insulin
release
 excitotoxic lesions of the lateral hypothalamus affect feeding area
but not general arousal because the dopaminergic axons that pass
through stay intact
lesions of the ventromedial hypothalamus produced overeating, stimulation
suppressed eating
 damage to surrounding areas is necessary to see the full effect
melanin-concentrating hormone (MCH) and orexin: produced by the lateral
hypothalamus, stimulates hunger and reduces metabolic rate, which
preserves the energy stores
 MCH seems to be more responsible for stimulating eating, low MCH
levels are correlated with eating less while higher levels are
correlated with overeating


low orexin levels are correlated with somewhat lower eating and
obesity later in adulthood, higher orexin levels just before mealtime
seems to be responsible for increased alertness and activity,
supposedly in preparation for the hunt for food, lower orexin levels
for the sleepiness experienced after mealtime
neurons have connections with the parts of the neocortex involved
in motivation and movement, as well as with the spinal cord
(presumably to control metabolic rate)
neuropeptide Y (NPY): neurotransmitter released in the arcuate nucleus of
the hypothalamus that stimulates frantic, ravenous eating, levels increase in
response to food deprivation and decrease in response to eating, thought to
be responsible for stimulating eating after food deprivation
 signals to stimulate glucoprivic eating are carried from NPY neurons
in the medulla to those in the arcuate nucleus
 ghrelin works by stimulating receptors on NPY neurons
 NPY neurons send signals to MCH and orexinergic neurons in the
hypothalamus, thought to be directly responsible for the stimulation
of eating, as well as to the paraventricular nucleus of the
hypothalamus, where presence of NPY affects metabolic functions
like the secretion of insulin
 NPY neurons also release agouti-related peptie (AGRP), which has a
similar effect
ghrelin sends signals to the mesolimbic system
endocannabinoids stimulate eating by increasing the release of MCH and
orexin
nonexercise activity thermogenesis (NEAT): involuntary activity, negatively
correlated with amount of fat tissue
 presence of orexin increases NEAT
efficient metabolism: people with this kind of metabolism have calories left
over that get deposited in their long-term reservoir
inefficient metabolism: people with this kind of metabolism store less in their
long-term reservoir
people whose ancestors evolved in a place where famine was more likely are
more likely to have efficient metabolisms
some obese people have a mutation in the gene that produces leptin or
leptin receptors

infusion of leptin greatly affects the weight of those people without
leptin, but not of those without leptin receptors
leptin resistance: ineffectiveness of leptin in some obese people caused by
differences in the effectiveness of the leptin transport system across the
blood-brain barrier
 people with efficient metabolisms would show more resistance to
high levels of leptin, allowing more eating to prepare for times
when food is scarce, whereas people with inefficient metabolisms
would be more sensitive to leptin as a short-term satiety signal
leptin increases the release of orexin
aged obese rats had a 50 percent reduction in leptin receptors
uncoupling protein (UCP): expression increased by the presence of leptin, its
expression increases metabolic rate
 higher levels of UCP in rats produced rats that were unusually lean
and ate more than normal
evidence that the symptoms of eating disorders are actually the symptoms
of starvation, which then propels the vicious cycle of the eating disorder

study of previously healthy young men forced to eat a diet of semistarvation for six months, started showing symptoms of anorexia
like preoccupation with food, ritualistic eating, erratic mood
changes, and impaired cognitive performance
 sight of food stimulated the anterior cingulate cortex in anorexic
patients, and they reported food as being more threatening than
controls
starving rats showed increased activity, perhaps reflecting an innate
tendency to increase activity in response to starvation to promote foodfinding behavior
 could also be an effort to keep warm
 NPY stimulates this wheel-running under conditions of starvation
bulimia is characterized by alternation between binge eating and extreme
dieting
 binge eating is followed by self-induced vomiting or use of
laxatives, accompanied by feelings of depression
 body weight can vary from overweight to underweight
women who have been fasting eat less than they otherwise would, while
men eat more
 possible explanation for why anorexia is more prevalent in women;
women don’t compensate for a period of food deprivation by eating
more
serotonin agonists help with bulimia but not anorexia
 behavioral therapy for anorexia: encourage patients to eat more
quickly, keep them in a warm room that keeps anxiety and activity
level low
Chapter 13
perceptual learning: allows us to identify and categorize objects and
situations, corresponds to changes in the sensory association cortex
stimulus-response learning: allows us to learn a specific behavior in
response to a certain stimulus, requires input from sensory systems and
their interaction with the environment
associative long-term potentiation: the synapse between the conditional
stimulus and response is at first weak, but becomes strengthened because of
its repeated activation at the same time as the synapse between
unconditional stimulus and response
 Hebb rule: learning results from the repeated activation of a
synapse when the postsynaptic neuron is firing
instrumental conditioning: learning an association between a response and a
stimulus, allowing the adjustment of behavior as a factor of response to that
behavior
 learning occurs through the synapses between motor networks
responsible for behavior and sensory networks responsible for
perception of the stimulus being strengthened
reinforcement: anything that promotes a certain behavior (can diminish
other behaviors as a result of one behavior increasing, but not the central
goal)
punishment: anything that decreases a certain behavior, necessarily
unpleasant (punishing)
motor learning: changes within the motor systems, necessarily incorporates
input from the sensory systems which provide information about the
environment
any kind of learning incorporates most or all of these kinds of learning

more complex learning also involves learning the relationships
between different stimuli
product of relational learning: hear a cat meowing in the dark and the tactile
and visual circuits associated with cats are stimulated in the somatosensory
and visual association cortices
episodic learning: learning distinct events that we witness, requires
remembering both the event itself and the order in which events occurred
long-term potentiation: repeated stimulation of a synapse causes a longterm increase in EPSPs in the postsynaptic neurons, cause of learning, takes
place on the dendritic spines of pyramidal cells
hippocampus: CA1-4 fields
hippocampal formation: hippocampus, dentate gyrus, and subicular complex
entorhinal cortex provides the primary input to the hippocampal formation
through the perforant path, where the axons synapse on the granule cells in
the dentate gyrus
 if LTP has taken place, the population EPSP of the perforant path
axons on the granule cells of the dentate gyrus will be greater than
it was before
dentate gyrus sends neurons to the pyramidal cells of the CA3 field, from
where one branch goes to the basal forebrain through the fornix, and the
other branch synapses on the pyramidal cells of the CA1 field, which
provides the main output of the hippocampus, to the subiculum, entorhinal
cortex, and basal forebrain
when neurotransmitters bind to the postsynaptic receptors of an alreadydepolarized dendritic spine, synaptic strengthening occurs
 but, synaptic stimulation and depolarization have to occur
simultaneously
 this is because if the dendritic spine is already depolarized and the
synapse is stimulated, magnesium is no longer blocking the calcium
channel of NMDA receptors and glutamate (also necessary to open
the calcium channels) is present
o calcium is a necessary second messenger to enact the
structural changes that allow LTP to occur
dendritic spikes: action potentials in the dendritic spine that only occur if the
axon of the neuron is already stimulated, can happen in the pyramidal cells
of field CA1
 simultaneous occurrence of an action potential and a dendritic spike
strengthens the synapse
 only happens with the conjunction of a strong synapse firing
elsewhere on the postsynaptic cell, because dendritic spikes have
high thresholds and therefore need a higher level of activation to
occur
o if they do become active, the calcium will enter those cells on
the dendritic spine, strengthening the synapse
strengthening of a synapse occurs when more AMPA receptors are inserted
into the postsynaptic membrane of the dendritic spine, which causes a larger
EPSP because AMPA receptors control sodium channels
 flood of AMPA receptors to the dendritic spine seems to be enacted
by CaM-KII enzyme, which is inactive until calcium binds to it, but
clustered in the postsynaptic dendritic spine after LTP had occurred
o CaM-KII is also capable of autophosphorylation, which means
that it can self-activate by attaching a phosphate group to
itself, without the presence of calcium
long-term depression: weakening of synaptic strength following lowfrequency stimulation of synapses that fail to depolarize the postsynaptic
membrane, important for memory by weakening some synapses while
others are strengthened
LTP causes both the change of shape of dendritic spines and their increased
production
nitric oxide synthase: an enzyme released by dendritic spines that diffuses
back to the presynaptic membrane and induces changes, like the release of
more glutamate, important for the establishment of LTP
 calcium-activated nitric oxide synthase is found in the hippocampal
formation
protein synthesis is necessary for LTP that lasts more than a few hours, that
which takes place in the first 45 days after the initial learning is necessary
for the formation of a good memory
LTP1: immediate strengthening of a synapse caused by the insertion of
AMPA receptors, lasts only a few hours
LTP2: longer-lasting LTP that involves local protein synthesis
LTP3: longest-lasting LTP that requires exportation of mRNA from the
nucleus to the dendritic spine for protein synthesis, as well as the presence
of dopamine
 plasticity-related proteins attach to specific dendritic spines where
LTP is taking place by means of chemical tags that indicate where
LTP is occurring
LTP varies depending on the part of the brain, LTP in field CA3 causes only
presynaptic changes (no changes to the dendritic spine) and only lasts a few
hours
re-activation of a pattern of activity of certain circuits constitutes recognition
of a stimulus
 can be specific to very precise neural circuits, e.g. only brain
regions corresponding to certain areas of the retina
area MT/MST of the brain was activated by still photos of people where
motion was implied, but not by those photos of people where motion wasn’t
implied
TMS of the ventral stream disrupted short-term memory retrieval of patterns
while TMS of the dorsal stream disrupted short-term memory retrieval of
location
 while short-term memories seem to reside in sensory association
cortex, prefrontal cortex is also important for their retrieval
in a memory task when people were required to manipulate the stimulus as
opposed to just remember it, the dorsolateral prefrontal cortex was
preferentially activated and people remembered the stimulus better later
information about the conditional and unconditional stimuli converge upon
the lateral nucleus of the amygdala
 synaptic changes in this area through LTP seem to correspond to
learning emotional responses
transcortical connections, along with the hippocampal formation, are crucial
for the recall of complex perceptual memories
basal ganglia takes over the enaction of certain behaviors once they become
automatic
destruction of the caudate nucleus and putamen interrupted capacity to
learn to make an operant response in monkeys, but not visual perceptual
learning
caudate nucleus and putamen receive lots of information from the cortex
about movements that are planned and provide output to the frontal lobe
through the internal globus pallidus and the thalamus
nigrostriatal system of dopaminergic neurons: connects the substantia nigra
with the striatum, important for movement
mesolimbic system of dopaminergic neurons: ventral tegmental area in the
midbrain, projects to the amygdala, hippocampus, and nucleus accumbens,
which projects to the basal ganglia, important for learning, cognition,
motivation and emotion
mesocortical system of dopaminergic neurons: ventral tegmental area to the
prefrontal and limbic cortices and the hypothalamus, important for learning,
reward, and desire
aversive and rewarding stimuli can both stimulate dopamine release,
dopamine is important for reward as well as for stress
activation of the reinforcement system relies on the stimulus being
unexpected, once learning is complete, only secretions of dopamine when
expected reward isn’t offered


if the stimulus is expected, learning doesn’t need to take place
people remembered words better when they were presented in
novel settings and the dopaminergic neurons were activated
 seems that the prefrontal cortex is responsible for detecting novel
situations and activating the learning system through its
connections with the ventral tegmental area, which it causes to fire
in bursts, which greatly activates the nucleus accumbens
Old and Milner: experiment where they stimulated the rat’s brain at each
place where they had to make a decision in a maze, found the rats kept
returning to those places, later found out that they were stimulating the
medial forebrain bundle, which connects the ventral tegmental area and
nucleus accumbens, same stimulation in humans causes reports of extreme
pleasure
nucleus accumbens: reward center of the brain, essentially an extension of
the striatum and often referred to as the ventral striatum
 activated by electrical stimulation of the ventral tegmental area or
the medial forebrain bundle, as well as cocaine, water, food,
money, and pictures of attractive members of the sex of sexual
desire
both the presence of dopamine and the activation of NMDA receptors in the
nucleus accumbens, lateral amygdala and prefrontal cortex are necessary for
instrumental conditioning to occur
hippocampal formation’s primary role in memory formation seems to be
consolidating short-term memories to long-term memories
sensory association cortex seems to be integral for declarative memory,
while the basal ganglia are necessary for non-declarative memory

EP had anterograde amnesia and was capable of learning word
associations, but was relying on his basal ganglia system and not
the normal declarative learning system, despite the response taking
the form of standard declarative memory
entorhinal cortex is the single most important input to the hippocampal
formation, specifically to the dentate gyrus, CA1 and CA3
 hippocampal formation also receives input from subcortical regions
through the fornix, including the dopaminergic neurons in the
ventral tegmental area, noradrenergic neurons in the locus
coeruleus, serotonergic neurons in the raphe nuclei,
acetylcholinergic neurons in the medial septum, and the
mammillary bodies
perirhinal cortex transmits information from the ventral stream,
parahippocampal cortex from the dorsal stream
Korsakoff’s syndrome, which causes severe anterograde amnesia, seems to
result from a deterioration of the mammillary bodies
 confabulation of stories that have true elements and acting on
those stories is symptomatic, thought to emerge from damage to
the prefrontal cortex and resultant failure to suppress past
memories when they’re evoked by present stimuli
input to the entorhinal cortex comes from the amygdala, limbic, perirhinal
and parahippocampal cortices, and association regions in the neocortex
a period of anoxia can quickly destroy area CA1, because glutaminergic
neurons release a high level of glutamate during periods of metabolic
disturbance, like anoxia, which stimulates the great number of NMDA
receptors in area CA1 and opens their ion channels to calcium and calcium
floods in, destroying the neurons
hippocampus receives input from sensory cortices and modifies the
connections that are being consolidated there based on that information
 the greater the damage to the hippocampal formation and
surrounding area, the farther back the retrograde amnesia goes,
shows that that system is still in some way involved in maintaining
and retrieving most of our memories, especially those that are
more complex and therefore require the establishment of more
connections
o as time goes on, responsibility for retrieving the memories is
shifted more and more to the prefrontal cortex
 hippocampus is especially (but not exclusively) important for the
formation of episodic memories, because they require so many
more connections to be formed, destruction of the hippocampus is
sufficient for anterograde amnesia of episodic memories,
destruction of surrounding cortex is necessary to prevent
consolidation of semantic memories as well
brain damage to memory systems early in life can have a lesser impact,
probably because other brain regions take over and compensate for the
damage
anterolateral temporal lobe seems to be important for storing semantic
information, although the hippocampal formation is still important for its
consolidation into memory
 double dissociation between retrograde amnesia and semantic
dementia
semantic dementia: damage beginning at the temporal lobe that progresses
to the frontal lobe, affecting the hippocampus on its path (though not
originating there)

fundamental misunderstanding of what objects are meant to do is
characteristic of the dementia
tasks requiring subjects to learn about the spatial relations between
landmarks activated the right hippocampal formation, while tasks requiring
subjects to simply learn a series of directions to navigate from one landmark
to the next activated the basal ganglia, demonstrating its reduction to a
simple response task
 rats with hippocampal lesions that are released from the same
place every time on the Morris Water Maze task are capable of
learning and decreasing the time necessary to find the platform,
while rats with the same lesion that are released from a different
location each time show no such learning curve
place cells: neurons that respond selectively to perception of an animal
being in a specific location, have spatial receptive fields, located in the
hippocampus

receive information from the parietal cortex via the entorhinal
cortex, which has something like spatial receptive fields, but not as
well defined as those of the hippocampus
 pyramidal cells in CA1 responded not only to the current location,
but the intended destination
o animals with field CA1 that didn’t have NMDA receptors
showed place cells with spatial receptive fields that were
much larger and less well-defined
evidence shows rehearsal of learned spatial relations during sleep, animals
in slow-wave sleep showed the same activation of place cells as when they
were learning a maze task
reconsolidation of memories requires LTP, and memories are therefore
vulnerable to be erased when they’re being recalled if LTP is somehow
blocked from happening before reconsolidation can occur (e.g. seizure,
blocking NMDA activity or protein synthesis)
hippocampus shows neurogenesis when activated by learning (e.g. spatial
relation task, not stimulus response), connections between new neurons
seem to be easier to form, unclear why neurogenesis only occurs in the
hippocampus and olfactory bulb
Chapter 14
people with right hemisphere damage have trouble talking about maps or
complex geometrical forms as well as using/manipulating them
function words: words with grammatical meaning but not much semantic
meaning (e.g. the, and), Broca’s aphasia patients have particular difficulty
producing these
content words: words with semantic meaning (e.g. apple, throw)
damage to the head of the caudate nucleus can produce a Broca’s-like
aphasia
agrammatism: symptom of Broca’s aphasia, difficulty using grammatical
constructions and extracting meaning if it’s dependent on grammar (e.g.
word order)
 Broca’s area was active when subjects had to learn complex
artificial grammar rules
voiced speech activated the periaqueductal grey matter and the auditory
cortex, auditory cortex involvement allows for feedback from own voice
allowing regulation of one’s own speech
anomia: symptom of all kinds of aphasia, difficulty finding words
 especially evident with Broca’s aphasia
 circumlocutions: roundabout ways of communication characterized
by people with anomia
 pure anomia (without any other symptoms) is produced by damage
to the left temporal or parietal lobe, sparing Wernicke’s area
 averbia: anomia for verbs in particular, produced by damage in and
around Broca’s area
apraxia of speech: also a symptom of Broca’s aphasia, difficulty with the
movements of the mouth and tongue necessary for speech, leading patients
to mispronounce words
 thought to be due to damage to connections with motor system
that controls movements necessary for speech, specifically in the
left precentral gyrus of the insula
pure word deafness: inability to understand spoken words despite having no
deficit in hearing, speech production, or comprehension of words by
modalities other than hearing, due to damage to Wernicke’s area or
disruption of input to the region
activity of areas of the brain that control speech production respond to
auditory input of speech, evidence of mirror neurons at work
 reading a verb produced activation in the motor cortex that controls
the relevant part of the body
temporo-parietal occipital juncture: relay point for words in the form of
auditory stimuli and the representation of those words in other sensory
modalities

transcortical sensory aphasia: condition of patients with damage to
this area, can repeat words but can’t understand speech or produce
meaningful speech of their own
 associations between words and representations in other sensory
modalities could be explained by the Hebb rule
memories of words in each sensory modality seem to be stored in the
sensory association cortex, where they’re then activated by hearing the
auditory stimulus that corresponds to a certain word
autotopagnosia: inability to name one’s own body parts due to damage of
the left parietal lobe
conduction aphasia: completely normal speech production and
comprehension except for an incapacity to repeat sentences word-for-word
due to damage to the arcuate fasciculus, especially pronounced for words
without semantic meaning
 presumably, pathway between the temporo-parietal occipital
juncture and Broca’s area carries information about the meaning of
the sentence
 information traveling back and forth along the arcuate fasciculus is
what’s known as the phonological loop in the working memory
model
Broca’s area seems to be responsible for inner speech, TMS of the area
disrupts covert as well as overt speech, also creates sensation of not being
able to get the word out
use of symbols by apes could be instrumental learning rather than a true
semantic understanding of the symbols, or a combination of both
two bonobos started training from a young age, partly by modeling the
behavior of their mother, who was undergoing language training

one of the bonobos, Kanzi, was particularly skilled, learned to
request things that weren’t there using lexigrams, and could carry
out spoken word instructions
o however, following instructions could be at least some degree
of instrumental conditioning, he would sometimes start to
carry out the command before the researcher had finished
saying it
Chapter 15
glioma: tumors arising from glial cells in the brain, neurons can’t become
tumors because neurons don’t divide
meningioma: tumors arising from the dura mater or arachnoid membrane
partial seizures: seizures restricted to a certain part of the brain and arising
from a specific focus, either scarred tissue or a developmental abnormality
 simple partial seizures: cause changes in but not loss of
consciousness
o seizures during sleep usually happen during REM, which can
cause the person to act out their dream, but is very different
from REM sleep disorders, seizure activity is a clear spike on
the EEG
 complex partial seizures: cause loss of consciousness
generalized seizures: seizures involving most of the brain, can sometimes
arise from a specific focus but where that focus is is not always clear
 grand mal seizures: characterized by convulsions because it
involves the motor area of the brain, most serious kind of seizure
o aura: before the grand mal seizure begins, provoked by
activity at the focus of the seizure and characterized by the
role of that focus (e.g. a limbic lobe focal point would provoke
an emotional aura)
 tonic phase: all the muscles contract
 clonic phase: muscles begin trembling and convulsing
rapidly, lasts about thirty seconds, after which point the
person starts breathing again and usually lapses into a
prolonged sleep
 excited firing spreads from the focal point to other

areas of the brain, tonic phase begins when it reaches
the motor cortex, then subcortical regions send
inhibitory messages, producing the clonic phase at first
and then finally the end of the seizure
 interruption of respiration causes a certain degree of
brain damage, especially in area CA1 in the
hippocampus
spells of absence: seizure disorder seen in children where the child
seems to be distracted for a few seconds, if undiagnosed, can lead
to problems in concentration and in school, can happen up to a
hundred times a day and usually stops during adolesence
status epilpepticus: series of seizures without regain of consciousness,
sufficient to cause brain damage to the hippocampus (through the release of
excess glutamate)
seizures can result from barbiturate or alcohol withdrawal because the NMDA
receptors have become accustomed to the drug’s inhibitory effects and
therefore are more prone to hyperexcitability (and therefore seizures)
scar tissue irritates surrounding brain tissue, causes excitability that spreads
to other regions, inhibitory mechanisms usually hold this excitability in
check, seizures occur when the inhibition isn’t sufficient
 inhibition suppresses the functioning of the brain area surrounding
the scarring, which impairs cognitive functioning even when the
person isn’t have a seizure
hemorrhagic strokes: bleeding from a blood vessel in the brain, which puts
pressure on the surrounding brain tissue and thereby damages it
obstructive/ischemic strokes: blockage of a blood vessel causing loss of
blood flow to a certain brain region




thrombus: blood clot that forms in blood vessels, blocking the
passage of blood
embolus: piece of material that’s carried through the blood stream
until it reaches an artery too small to pass through and blocks it
ateriosclerosis: thickening of the arterial wall, preventing blood flow
brain damage occurs because the lack of glucose causes the
sodium-potassium pump to stop functioning and therefore the
membrane to become depolarized, triggering the release of
glutamate, causing more inflow of sodium and calcium ions, causing
the cell to take on water and swell, and calcium-activated enzymes
to destroy certain organelles, and the damaged mitochondria
release free radicals, which destroy everything
tPA: helps dissolve blood clots up to nine hours after the stroke but also
contributes to excitotoxicity if it’s allowed to cross the blood-brain barrier,
which will happen if the blood-brain barrier has been damaged by the stroke
desmoteplase: helps prevent clotting and isn’t a neurotoxin
fetal alcohol syndrome: abnormal facial development and deficient brain
development caused in the fetus of a mother who consumes alcohol while
pregnant
 neural adhesion protein: guides growth of developing neurons,
thought to be disrupted by the presence of alcohol
 alcohol also may interfere with neuroplasticity in the child’s brain
 study of Verbet monkeys on St. Kits island showed fetal alcohol-like
symptoms in children with mothers who drank alcohol while
pregnant
phenylketonuria (PKU): inherited lack of an enzyme to convert phenylalanine
into tyrosine, causing excess phenylalanine to interfere with the myelination
of the brain, which happens mostly during infancy, causes brain retardation
unless the infant is fed a low-phenylalanine diet
 if a mother has it, has to eat a low-phenylalanine diet while
pregnant in order to not interfere with the fetal brain development
Tay-Sachs disease: lack of certain lysosomic enzymes causing the lysosomes
in the brain and therefore brain tissue itself to swell, which leads to brain
damage
Down syndrome: congenital disorder resulting from an extra twenty-first
chromosome, causing physical abnormalities as well as smaller frontal lobes,
less gyri and sulci, and thin superior temporal gyri
 show brain degeneration at about the age of thirty analogous to
that of Alzheimer’s patients
prion proteins: proteins found in neuronal membranes that are resistant to
enzymes that normally break down proteins as well as to denaturing by
heat, thought to play a role in neural development in fetuses and
neurogenesis in adults (and therefore hippocampal long-term potentiation)
 transmissible spongiform encephalopathy (TSE): neurodegenerative
disorder causing large parts of brain tissue to die causing dementia,
speech impairment, ataxia, seizures, and trouble swallowing,
transmitted by introduction of misfolded prions (PrPSc) to normal
cells, which then causes the other, normal prions to become
misfolded
o can also be genetic, caused by a mutation in the gene that
codes for the prion protein
o just the presence of the PrPSc doesn’t cause TSE if they have
no normal prions to convert, thought that the mass
proliferation of misfolded prions triggers apoptosis
o bovine spongiform encephalopathy (mad cow), CreutzfeldJakob disease (human form of mad cow), Kuru, and scrapie
are all forms of TSE
Parkinson’s disease: near-disappearance of nigrostriatal dopaminergic
neurons causing an imbalance in the pathways of the internal and external
globus pallidus and therefore poverty of movement and difficulty initiating
movement









mostly not genetically determined, but can result from certain
genetic mutations
Lewy bodies: aggregations in the cytoplasm of the surviving
dopaminergic cells caused by abnormal accumulation of -synuclein
-synuclein: protein involved in synaptic transmission in
dopaminergic neurons, mutation causes aggregations in
dopaminergic neurons that interfere with their function
parkin: gene that’s responsible for carrying misfolded proteins to
proteasomes, which destroy them, doesn’t function properly when
mutated causing misfolded proteins to accumulate, which is
specifically disastrous to dopaminergic neurons
sporadic instances of Parkinson’s seem to arise from environmental
factors
L-DOPA: precursor to dopamine, increases dopamine concentration
in the brain and helps with Parkinsonian symptoms to a certain
extent, but only as long as the person’s brain has enough dopamine
receptors
MAO-B: enzyme that breaks down dopamine and releases hydrogen
peroxide, which can damage cells, inhibition of MAO-B is thought to
help prevent Parkinson’s/deal with Parkinsonian symptoms
tried implanting fetal tissue from the substantia nigra to the
putamen and caudate nucleus of Parkinson’s patients, helped
patients who had been responding to L-DOPA and therefore had a
sufficient number of dopaminergic neurons left to respond, some
patients also had painful invonluntary movements and so the
treatment was discontinued
neural stem cells implanted into the caudate nucleus in monkeys
differentiated into dopaminergic neurons as well as astrocytes and
other glial cells, had a positive therapeutic effect overall on the
monkeys’ motor control
 pallidotomy: destruction of the GPi causes less inhibition of the
motor cortices and therefore less poverty of movement, shows
similar effect with destruction of the subthalamus
case of the frozen addicts: seven young adults across California presented
with Parkinsonian symptoms, had all taken synthesized heroin that
contained MTPT, which causes cell loss in the substantia nira
Huntington’s disease: hereditary disorder caused by a misfolded protein
triggering apoptosis and thereby degeneration of the caudate nucleus and
putamen causing involuntary jerky movements, degeneration of the brain,
and eventual death
 starts with damage to GABAergic neurons in the putamen, which
removes inhibitory control on the motor cortices
 huntingtin (htt): protein that’s misfolded in Huntington’s patients,
normally the protein facilitates the production and transport of a
chemical called BDNF that’s necessary for the survival of neurons in
the caudate nucleus and putamen

possible treatment for Huntington’s is the introduction of RNA that
blocks the transcription of mutated htt into the striatum
Alzheimer’s disease: degeneration of the hippocampus, entorhinal cortex,
association cortex of the frontal and temporal lobes, the nucleus basalis,
locus coeruleus, and raphe nuclei
 amyloid plaques: protein core of -amyloid surrounded by
degenerating axons and dendrites, which are eventually destroyed
by glial cells leaving only the protein core
o caused by a larger-than-normal proportion of the long form of
the protein cut from the -amyloid precursor protein (APP),
which is more likely to be misfolded, too many misfolded A


proteins causes the cell to die
 chromosome 21 contains the gene that’s responsible for
producing APP, abnormal forms of APP cause the long
form of the protein to be produced preferentially,
increases the risk of developing late-onset Alzheimer’s
o seen in brains of Down’s syndrome patients too
neurofibrillary tangles: twisted filaments of tau protein, which is
normally a component in microtubules but change structure with
the progression of Alzheimer’s, causing cell death because of the
disruption of transport within the cell
only approved treatments are ACh agonists and NMDA antagonists
o research looking into drugs that enhance the destruction of
A, accumulation of the protein is thought to be the primary
source of neural degeneration
amyotrophic lateral sclerosis (ALS): degeneration of the spinal cord and
cranial nerve motor neurons, causes death within ten years of its onset due
to failure of the respiratory muscles
 hereditary cases are a result of the mutation of a gene on
chromosome 21 causing protein misfolding, impaired axonal
transport, mitochondrial dysfunction, and excitotoxicity in motor
neurons
 sporadic cases seem to arise from faulty RNA editing leading to
excitotoxicity in neurons with AMPA receptors
 possible treatment by injection of a protein that delays the death of
damaged motor neurons
multiple sclerosis (MS): interruption of the myelination of axons caused by
the immune system attacking myelin sheaths, thought to be related to the
contraction of an infection, either by the person themselves or by their
mother while she was pregnant
 progression of the disease is characterized by new symptoms
followed by partial recovery
 interferon : protein that modulates immune response, provides
some relief

glaitramer acetate: mixture of synthetic peptides that indirectly
suppresses activity of immune cells attacking the myelin sheath
Korsakoff’s syndrome: brain degeneration, particularly in the mammillary
bodies, that causes anterograde amnesia, caused by thiamine deficiency
resulting from prolonged alcoholism
 alcoholism interferes with the absorption of thiamine and makes its
consumption less likely given the amount of calories an alcoholic
gets from alcohol
herpes encephalitis: spreading of the herpes virus to the brain, where it
attacks the frontal and temporal lobes
polio: virus that causes damage to the motor neurons in the brain and spinal
cord
rabies: virus passed from the saliva of an infected animal, attacks cells in
the cerebellum and hippocampus
AIDS: when it affects the brain, causes damage to the hippocampus,
cerebral cortex, and basal ganglia by causing apoptosis of neurons in those
areas
meningitis: inflammation of the meninges caused by virus or bacteria,
causes damage to the brain by interfering with blood circulation or causing
hydrocephalus by blocking the subarachnoid space
Chapter 16
positive symptoms of schizophrenia: symptoms that exceed normally
cognition/cognitive processing, thought to be caused by overactivity of
dopaminergic neurons between the ventral tegmental area and the nucleus
accumbens and amygdala
 thought disorder: disordered, irrational thinking, not problems with





understanding or producing speech, but rather the thoughts that
underlie speech
o jumping from topic to topic could be a combination of this and
the negative symptom of a failure to maintain attention
delusions: beliefs that are contrary to fact
o erotomania: delusional belief that someone (usually of higher
social status) is in love with them
hallucinations: perceptions of stimuli that aren’t present
chlorpromazine: a dopmine-receptor blocker that’s used to treat
these symptoms
thought that these symptoms arise from the reward system
becoming active inappropriately, reinforcing irrational thought
patterns
o amphetamine causes the release of more dopamine in the
striatum in schizophrenic patients than in normal patients,
and a greater release of dopamine was correlated with the
incidence of positive symptoms
tardive dyskinesia: inability to inhibit movements resulting from the
supersensitivity of dopamine receptors after being blocked by
antipsychotic medication
negative symptoms: symptoms characterized by a lack of or deficit in
normal cognitive functioning, like flattened affect, poverty of speech,
anhedonia, social withdrawal, common to many of the neuropsychological
disorders, not just schizophrenia
 administration of indirect NMDA agonists has been shown to relieve
these symptoms
cognitive symptoms: deficits in cognition like difficulty with attention, deficits
in learning, memory, problem solving, and abstract thinking, and decreased
speed in limb and digit manipulation (psychomotor functioning), common to
many of the neuropsychological disorders, not just schizophrenia
a predisposition to schizophrenia seems to be heritable, but needs to be
combined with environmental factors as well
 children of discordant monozygotic twins are equally likely to be
affected, children of the affected twin of discordant dizygotic twins
are much more likely to be affected
 mutations in a wide variety of genes that are responsible for neural
differentiation and growth as well as development of axonal
connections during development seem to be the precursors for
schizophrenia
schizophrenic patients have ventricles nearly twice the size of those of
controls
seasonality effect: people whose mothers were pregnant during flu season in
the Northern hemisphere were more likely to become schizophrenic,
contraction of a virus during the pregnancy could have affected brain
development
 also, living in cities, both pre- and postnatally
 Vitamin D- and thiamine-deficiency also might play a role
deprivation of blood supply to the uterus due to complications in the
pregnancy or birth correlates with development of schizophrenia,
presumably due to its effect on brain development
evidence of some degree of lesser sociability and lower psychomotor
functioning in children who later developed schizophrenia, suggests that
there are some differences in the brains of schizophrenics even before they
start to display the standard symptoms of schizophrenia in early adulthood
in twins discordant for schizophrenia, the schizophrenic twin had larger
ventricles and smaller limbic lobes
concordance rate of schizophrenia for twins that shared a single placenta is
higher than that of twins with two separate placentas
schizophrenia is characterized by a sudden, rapid loss of brain tissue in early
adulthood, but no continuing degeneration afterwards, thought to be
triggered by the developmental changes in adolescence, which includes the
pruning of neural circuits
hypofrontality: decreased activity of the frontal lobes, particularly of the
dorsolateral prefrontal cortex, causing decreased performance on executive
functioning tasks
 thought to be due to a decrease in the metabolic rate of the
prefrontal cortex because of decreased activation of NMDA
receptors and therefore decreased dopaminergic activity, which
then causes hyperactivity of the striatum because the prefrontal
cortex is exerting less inhibition on it by means of the ventral
tegmental area
 symptom of schizophrenia, thought to be responsible for negative
symptoms
decreased dopaminergic activity in the prefrontal cortex causes increased
dopaminergic activity in the nucleus accumbens through its circuit through
the ventral tegmental area
 projections from the prefrontal cortex synapse on dopaminergic
neurons in the ventral tegmental area as well as on GABAergic
neurons, which then normally inhibit the nucleus accumbens
 don’t inhibit it if there’s hypofrontality, causing hyperactivity of the
mesolimbic pathway, which causes positive symptoms
chloropromazine: drug initially used to reduce brain swelling following
surgery, found to relieve the positive and negative symptoms of
schizophrenia to the extent where they didn’t have to be permanently
institutionalized, works as a dopamine antagonist
haloperidol: treatment for the positive symptoms of schizophrenia, binds to
D2 but not D1 receptors, D2 receptors are found in the nucleus accumbens
and striatum, while D1 receptors are found in the prefrontal cortex
 symptoms of schizophrenia are thought to arise from hyperactivity
of D2 but not D1 receptors
use of partial dopamine agonists are useful in the treatment of
schizophrenia, because they act as agonists where dopaminergic activity is
too low and antagonists where it’s too high
bipolar disorder: affective disorder characterized by the sequence of manic
and depressive episodes
major depressive disorder (MDD): depressive episodes that are continuous
or broken up
atypical depression: characterized by weight gain, insomnia, decreased
autonomic response to stress, seems to respond better to MAO-Is
MAO inhibitors: inhibit the activity of MAO, which destroys excess
monoamines (dopamine, norepinephrine, serotonin) and therefore acts as a
monoamine agonist, sometimes used to treat depression but can have
harmful side effects
trycyclic antidepressants: SSRIs/SNRIs, work by inhibiting serotonin and
norepinephrine reputake, don’t have MAO inhibitors negative side effects
 use of SSRIs or SNRIs depends on the side effects and response of
individual patients, not any inherent difference in effectiveness
o take about two weeks to kick in, could e due to the time it
takes for serotonin autoreceptors to change, inhibition of
those autoreceptors gets rid of delay
electroconvulsive therapy (ECT): electrical stimulation of the patient’s brain
while they’re anesthetized causing an increase in the release of GABA, used
to treat the affective disorders if other treatments don’t work, although longterm ECT causes brain damage
subgenual anterior cingulate cortex: area in the medial prefrontal cortex that
shows decreased activation in depressed patients, its stimulation with
electrodes, causing decreased activity, has been shown to help with
depression
 seeming discrepancy hasn’t been explained
 lesions result in a failure to extinguish classically conditioned
responses in rats, therefore seems to play a role in emotional
inhibition
vagus nerve: has afferent connections with the brain stem, its stimulation,
causing decreased activation, has been shown to help with depression
depressed patients have higher-than-normal levels of glutamate, NMDA
antagonists might help to treat it
lithium: used to treat the manic phases of bipolar disorder, which also
effectively eliminates the depressive phases, very effective, but has a low
therapeutic index, making the risk of overdose high, and a number of
adverse side effects (e.g. nausea, diarrhea, motor incoordination, etc.),
seems to work by stabilizing receptors in the brain (especially serotonin
receptors)
study showed that the presence of serotonin in the brain was necessary for
the success of at least some brands of depression treatment, but lower
levels of serotonin in the brains of non-depressed controls with no family
history of depression had no effect
depressed patients show increased activity of the amygdala, specifically
when they were asked to recall sad episodes from their lives
 also showed deficits on executive functioning and verbal memory
tasks
5-HT transporter (5-HTT): serotonin transporter located on chromosome 17
with either a short or long promoter region, people with one or two short
alleles and a greater number of stressful life events show a greater likelihood
of developing major depression than those without the short alleles
 people with two long alleles were more likely to respond to
treatment or even to a placebo
 short allele means fewer transporters and therefore less reuptake of
serotonin, thought to be associated with major depression because
an excess of serotonin during brain development causes decreased
development of the amygdala and subgenual ACC
o normally, there’s a strong positive correlation between
amygdala and subgenual ACC activity, and between the
subgenual and dorsal ACCs and a negative correlation
between amygdala and dorsal ACC activity, these correlations
aren’t as strong in people with two short alleles
interruption of neurogenesis may play a role in the affective disorders,
treatments for the disorders also increase neurogenesis, and they lose their
effectiveness if neurogenesis is blocked during treatment
REM sleep deprivation over several weeks relieves the symptoms of
depression
total sleep deprivation has immediate anti-depressant effects in two thirds of
patients, most effective on patients that feel worst in the morning and feel
better as the day goes on
 depressed patients have abnormal amounts of REM sleep and
almost no slow wave sleep, some anti-depressants suppress REM
sleep
o sleep deprivation increases the proportion of slow wave sleep,
because it’s a more efficient kind of sleep

thought that sleep causes the brain to produce a depressogenic
chemical
seasonal affective disorder (SAD): depression induced by the winter season,
characterized by lethargy and sleep disturbances, as well as weight gain,
appears to have a genetic basis
 thought to be due to decreased sensitivity to zeitgebers and
therefore needing a stronger-than-normal zeitgeber to reset their
circadian rhythm
o people with SAD show a longer-than-normal delay between
the onset of melatonin secretion and the midpoint of sleep

phototherapy: exposure to bright light for several hours a day,
treatment for SAD
Chapter 17
anxiety is adaptive if there’s a valid source of anxiety that needs to be dealt
with, anxiety disorder is the experience of maladaptive anxiety
panic disorder: anxiety disorder characterized by periodic attacks of acute
terror lasting for seconds to hours
generalized anxiety disorder: excessive anxiety and worry to the point that it
interferes with day-to-day life
social anxiety disorder: excessive fear of interactions and scrutiny of others
leading to the avoidance of social situations, particularly those requiring
performance of one sort or another
anticipatory anxiety: fear of having a panic attack, leads to comorbidity with
other disorders, like agoraphobia
lactic acid and air with elevated levels of CO2 increase heart rate and rate of
respiration, can trigger a panic attack
anxiety disorders have a hereditary component, short allele for 5-HTT is also
associated with higher levels of anxiety and increased amygdala activation in
anxiety-provoking situations
 another possible cause is decreased sensitivity or decreased
numbers of benzodiazepine receptors
SSRIs are effective in treating panic attacks through their effect on 5-HT1A
receptors

targeted mutation of these receptors in embryos leads to anxious
behavior in adulthood, but mutation against them during adulthood
has no effect on anxiety
o serotonin has different effects on the brain at different points
during development
the amygdala and the cingulate, prefrontal, and insular cortices are all
implicated in panic attacks and their level of activation is positively
correlated with experience of anxiety
 benzodiazepines: help with anxiety because they stimulate GABAA
receptors, which have a high concentration in the amygdala
o can become addictive, also treat panic induced by
hallucinogen intoxication
 administration of indirect agonists of NMDA receptors has also
helped with treatment of phobias and anxiety disorders in
conjunction with behavioral therapy
obsessions and compulsions are characteristic of schizophrenia as well as
obsessive-compulsive disorder, but people with OCD recognize the
senselessness of the compulsions while schizophrenics don’t
compulsions seem to be the exaggeration of normal, species-typical
behaviors
at least some hereditary basis for OCD that seems to link it with Tourette’s
syndrome
 Tourette’s syndrome: neurological disorder characterized by
muscular and vocal tics, leading to periodic shouting, often of
obscenities
can also be caused by brain damage, specifically to the basal ganglia,
cingulate gyrus, or prefrontal cortex
 -hemolytic streptococcal infection: infection that can trigger auto-

immune diseases that attack different parts of the body including
the brain, OCD patients who had this infection during childhood
showed enlarged basal ganglia
deep brain stimulation of the basal ganglia has been shown to help
with symptoms of OCD, correlation between hyperactivity of the
basal ganglia and OCD symptoms
symptoms of OCD may be due to overactivity of the direct pathway, which is
responsible for learning and carrying out automatic behaviors, which are
then inhibited by the indirect pathway when they’re not adaptive
 overactivity could overcome this inhibition and be responsible for
the overabundance of these automatic behaviors
 serotonin’s effectiveness as a treatment could be due to its
inhibitory effect on species-specific bheavior
increased activity in the caudate nucleus and orbitofrontal cortex were
associated with obsessive thoughts, and improvement was correlated with
lower activity in these areas
ventral hippocampal lesions causes an incapacity to inhibit responses in rats,
effect goes away with SSRIs and is enhanced by dopamine agonists
 unclear where the drugs are having this effect
SSRIs are more effective than SNRIs in treating compulsive symptoms of
OCD
cingulotomy: destruction of the cingulum bundle, which connects the
prefrontal and cingulate cortices with the limbic cortex and basal ganglia,
helps with OCD but can cause apathy and problems with planning or
inhibiting socially inappropriate behavior
capsulotomy: destruction of the internal capsule, which connects the
caudate nucleus with the medial prefrontal cortex, has the same effects and
side effects as the cingulotomy
indirect NMDA agonists also helped with OCD symptoms when combined
with cognitive therapy, possibly helps with the distinction of the maladaptive
behavior as it helps with the extinction of phobias and anxiety
autistic disorder: deficit in the development of social interaction and
communicative ability, combined with engaging in repetitive and stereotyped
behavior


language development in people with severe autism is abnormal,
fail to use language productively/creatively
seems to be correlated with mental development abnormalities that
preclude the development of theory of mind
o because of this, children with autism don’t show pretend play
o right medial prefrontal cortex seems to be important for
theory of mind
brain abnormalities seen in autism can be caused by prenatal infections that
affect brain development
 prenatal thalidomide: drug prescribed to pregnant women to
combat morning sickness, discontinued because it has been
associated with birth defects in children
 autistic brains grow abnormally quickly between two and three
years of age and then slows down, so it’s only slightly larger than
normal by adolescence
o abnormality specifically in the frontal and temporal cortices
o enhanced early development seems to cause a greater-thannormal number of short-range axons, which could account for
the savant syndrome, and the poverty of long-range axons
later on
concordance rate for autism was much higher in monozygotic twins, and the
non-affected twin in discordant monozygotic twins showed deficient
language development and social withdrawal
activation of the right superior temporal sulcus and medial prefrontal cortex
in autistics was much less than that of controls during a task involving
animated shapes, seems to be important in determining the intentions of
others

fusiform face area activation was also lower when looking at faces,
suggests that not spending as much time looking at faces caused it
not to differentiate into an area of expertise for faces
 also, lower activation in mirror motor neurons and thinner cortex of
the mirror neuron system
 auditory cortex in autistics didn’t show differential activation to
speech sounds, as did that of controls
increased volume of caudate nucleus in autistics was correlated with
prevalence of stereotyped behaviors, shows parallel with the role of the
caudate nucleus in OCD
 SSRIs have been shown to reduce some of this stereotyped
behavior in autistic patients
Asperger’s disorder: milder form of autism, characterized by deficits in social
interaction and stereotyped behaviors, but without a delay in language
development or the cognitive deficits
children with ADHD are more likely to grow up to develop antisocial
personality disorder and substance abuse
 most common treatment for ADHD is a dopamine agonist, moderate
levels of the drug seem to inhance dopaminergic and noradrenergic
transmission in the prefrontal cortex, while higher levels of the drug
suppressed activity
 seems to be due to a problem in dopaminergic transmission that
causes immediate reinforcement to be even more reinforcing and
for delayed reinforcement to become more rapidly less reinforcing
than in a normal person
stop signal task: task that requires inhibition of an already-initiated task,
subjects with ADHD show severe impairment, and the unaffected siblings of
subjects with ADHD show performance somewhere between that of people
with ADHD and controls
 capacity for inhibitory control may have a genetic basis
ADHD is characterized by symptoms similar to those of people with
prefrontal damage, including distractability, impulsiveness, poor planning,
and hyperactivity
 caudate nucleus and medial prefrontal cortex showed lower
activation in people with ADHD for tasks that required inhibition and
attention than in controls, presumably affected by the abnormal
dopaminergic transmission
 conduct disorder: patterns of activity that disrupt expected social
norms (e.g. vandalism, theft), seen in adults who had ADHD as
children
initially, cortical growth of children with ADHD lags behind that of their
peers, but it eventually catches up
Chapter 18
dopamine release in the nucleus accumbens is a sufficient but not necessary
condition for reinforcement to occur
 opiates don’t rely on this system for their reinforcing quality
a single administration of a drug that stimulates dopamine release resulted
in stronger excitatory connections in the ventral tegmental area, increasing
activation in brain areas connected to the VTA, including the nucleus
accumbens in the ventral striatum

dorsal striatum: caudate nucleus and putamen, responsible for
drug-taking becoming habitual after changes in the ventral striatum
occur as an immediate response to the drug’s effects, responds to
stimuli associated with drug-taking
 reinforcing quality of drugs relies on the circuit between the VTA
and NAC
 as drug use increases, response to naturally reinforcing stimuli
decreases
negative reinforcement: achieved when a behavior eliminates or reduces an
aversive stimulus, increases the likelihood of that behavior
punishment: achieved when a behavior induces an aversive stimulus,
decreases the likelihood of that behavior
the addictiveness of drugs relies on their initial positively reinforcing effect of
being pleasant, activating the reward circuit, and later, on their negatively
reinforcing effect of removing withdrawal symptoms
 tolerance: decreased sensitivity to the effects of a drug after
continued use
 withdrawal: opposite effects of the drug, brought on by stopping
taking a drug after prolonged use
people who use drugs without becoming addicted presumably rely on their
higher cognitive centers to inhibit the drug-taking behavior despite its
reinforcing quality, in addicts, this inhibition isn’t strong enough to stop the
behavior
incentive salience: the character of stimuli present at the time that the drug
activates the reward pathway and provoke craving, emotional context can
also have incentive salience
 this effect relies on dopaminergic activity in the NAC and VTA, and
is abolished with stimulation of the ventromedial prefrontal cortex

or inhibition of the dorsal anterior cingulate cortex
o dACC has excitatory connections with the NAC and plays a
role in initiating craving, while the vmPFC plays a role in the
inhibition of its effect
model of craving in animals: rat learns to press a lever when a light
is present to get a drug, response is extinguished, then the rat is
given a free shot of the drug or the light is shone again, reinstates
the behavior
o doesn’t occur if dopamine transmission in the NAC is blocked
ACC and orbitofrontal cortex are most often stimulated by the administration
of drugs of abuse or stimuli associated with them, less often, the insula and
dorsolateral prefrontal cortex
 only the ACC was activated by alcohol or stimuli with incentive
salience related to alcohol in controls, but the NAC, ACC, VTA, and
insula were all activated in response to the same stimuli in
alcoholics
prefrontal activation and performance on tasks requiring the prefrontal
cortex is negatively correlated with degree of cocaine abuse

also showed structural abnormalities in the area as well as in the
superior temporal cortex
 correlation, not clear if cocaine abuse caused the degeneration
 thought to be related to the high level of comorbidity between
substance abuse and schizophrenia, which is also characterized by
hypofrontality
 children who scored lower on behavior inhibition tasks were more
likely to develop substance abuse problems in adulthood
stress makes rats more likely to abuse cocaine if given the opportunity, and
rats in infancy were more likely to abuse it later in life
opiate receptors in the periaqueductal grey matter are responsible for
opioids’ analgesic effects, and those in the VTA and NAC for its reinforcing
effect, doesn’t rely on dopamine release
  and  opiate receptors are responsible for reinforcing and
analgesic effects
release of dopamine and endogenous opioids are necessary for
reinforcement to occur
place preference test: test that trains the rat to associate a particular place
with the administration of a particular drug
antagonist-precipitated withdrawal: withdrawal symptoms produced by
blocking certain receptors, for morphine-addicted rats, the most powerful
withdrawal symptoms were produced by blocking opiate receptors in the
locus coeruleus and the periaqueductal grey matter, and caused increased
levels of glutamate in the locus coeruleus
cocaine blocks dopamine reuptake, while amphetamine blocks its reuptake
and stimulates its release from terminal buttons


both stimulate dopamine release in the NAC
can cause the positive symptoms of schizophrenia, presumably
because both are characterized by an increased presence of
dopamine
 prolonged use of these drugs causes a decrease in dopamine
receptors in the ventral striatum even after abstention for many
years, increases susceptibility to Parkinson’s
 methamphetamine can provoke apoptosis of serotinergic neurons in
the cerebral cortex, striatum, and hippocampus
nicotine stimulates nicotinic acetylcholine receptors and triggers dopamine
release in the NAC
 reinforcing effect of nicotine seems to be caused by the activation
of nicotinic receptors in the VTA
 rimonabant: drug that blocks CB1 receptors and reduces nicotine
self-administration in rats, thought that the CB1 receptors stimulate
the release of dopamine in the NAC, has been used to help people
quit smoking
nicotinic receptors open calcium channels in response to the presence of
ACh, then close as ACh is destroyed, or become desensitized to the effect of
ACh

prolonged presence of nicotine in the brain initially stimulates these
receptors and then causes most of them to become densensitized,
which also causes the number of nicotine receptors to go up over
time
 cigarettes are most pleasurable after a period of abstinence (like
overnight) because the nicotine receptors have become sensitized
again
insula damage has been correlated with greater ease and success in quitting
smoking
nicotine suppresses appetite by inhibiting the release of melanocyteconcentrating hormone from the lateral hypothalamus
alcohol is an indirect GABAA agonist and an indirect antagonist of NMDA
receptors, both of which can trigger apoptosis and therefore brain damage if
the effect is widespread enough
 alcohol is anxiolytic in its effect of reducing the punishing effect of
aversive stimuli, reduces the inhibition that would normally be





provoked by their administration, thought to be due to its agonizing
effect on GABAA receptors
increases release of dopamine in the NAC
haloperidol: drug that blocks dopamine receptors, reduced the
reinforcing effects of alcohol consumption
its NMDA antagonizing effect reduces LTP in the hippocampus and
therefore interferes with learning
sudden cessation of alcohol consumption causes increased activity
of NMDA receptors, which inhibit dopamine release in the VTA and
NAC, and can also cause seizures through their overexcitability
following the release from long-term inhibition
drugs that block opiod receptors block the reinforcing effect of
alcohol, abstinence from alcohol in alcoholics showed a correlation
between increase in  receptors in the NAC and intensity of craving
cannabis binds to CB1 receptors, supposedly responsible for the high that it
produces, and also acts on dopaminergic receptors in the NAC, increasing
dopamine release
 its excessive activation of CB1 receptors in the hippocampus
interferes with normal memory formation
environment seems to determine whether a person will initially try a drug,
while genetics determine whether they will abuse it
 increased sensitivity to environmental stressors may increase the
likelihood of abuse of alcohol as an anxiolytic
 variations in the genes that code for the  receptor and GABAA
receptor have been associated with the likelihood of alcohol
dependence
methadone works by slowly activating opiate receptors in the brain, and
activating them over a long period of time, meaning heroin won’t produce a
high

only true if it’s administered orally, therefore that’s the only form
it’s stored/available in
bupreorpine: partial agonist for the  receptor, occupies the space but
activates it less than a normal opiate would, blocks the effect of opiates
without producing the same effect, produce reports of decreased craving
opiate antagonists will block the effects of heroin, but increase craving for it
rats with immune systems stimulated to produce antibodies to cocaine
showed less sensitivity to cocaine and less cocaine in their brains after an
injection
 experimental trials in humans have shown promising effects
GABA agonists cause a reduction in the release of dopamine in the NAC after
a cocaine injection
addiction to smoking seems to be a combination of addiction to nicotine as
well as the sensory effects produced by smoking
bupropion: catecholamine (dopamine, norepinephrine) agonist that caused
less activation of the medial prefrontal cortex when presented with stimuli
with incentive salience related to smoking and reported less craving
varenicline: partial nicotinic agonist that’s been shown to facilitate
abstinence from smoking
naltrexone: opiate antagonist that inhibits the reinforcing effects of alcohol
and increases the likelihood of successful abstinence from drinking and
decreased craving when combined with behavioral therapy
acamprosate: NMDA antagonist that causes smokers to be less likely to start
drinking again, shown to be very effective with combined with naltrexone to
help recovering alcoholics quit