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Origins of Biopsychology
I.
II.
III.
IV.
Introduction
Course Overview
History of Behavioral Neuroscience
Course Goals
Biopsychology
• Seeks to describe the physiological
mechanisms of the body that mediate our
movement and mental activity.
• “Mental activity” includes a vast array of
things including feeling, thinking,
consciousness, communication, learning,
and memory.
• A.k.a. psychobiology or behavioral
neuroscience
Topics to be Covered
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History
The Neuron
Brain Structures
Drugs
Sensation (vision,
etc…)
• Sleep
• Eating and Drinking
• Learning and Memory
• Language and
Communication
• Psychological
Disorders
• Emotions (if extra
time at the end)
Two Sides to the Mind-Body
Question
• Dualism: The belief that the mind and body (or
the mind and the brain) are separate entities.
– Often assumes the existence of a non-material soul
or spirit
– Most popular view throughout history
– May be “wired” to view ourselves this way
• Monism: The belief that the mind and body (or
the mind and the brain) are one.
– Mind and brain are almost synonymous
– The mind is a product of the brain
– Most common view among biopsychologists
III. History of Behavioral
Neuroscience
A. Aristotle (384-322 BC)
– dualist
B. Hippocrates (460-370 BC)
– monist
C. Descartes (17th Century)
– modified dualist
D. Galvani (17th Century)
– frog muscles contract with electricity
III. History of Behavioral
Neuroscience (Continued)
E. Muller (19th Century):
–
–
doctrine of specific nerve energies
advocate of experimentation
F. Flourens (19th Century)
–
experimental ablation
G. Broca (19th Century)
–
aphasia
H. Fritsch and Hitzig (19th Century)
–
I.
stimulation of dog cortex produces body movement
Darwin and Wallace (19th Century)
–
theory of evolution and common descent
Lateralization of Function versus
Localization of Function
• Localization of Function: The tendency for
a function to be located in a particular area
of the brain (i.e., a great deal of advanced
visual processing occurs in the occipital
lobe).
• Lateralization of Function: The tendency
for a function to be primarily located on
one side of the brain (i.e., Broca’s area is
typically in the left frontal lobe).
Cells of the Nervous System
I.
II.
III.
IV.
V.
VI.
VII.
Introduction
Neurons
Ways of Classifying Neurons
Nervous System Support Cells
Communication Within a Neuron
Communication Between Neurons
Major Neurotransmitters
How Long Would it Take to Count
to 100 Billion?
• 60 seconds per minute × 60 minutes per
hour × 24 hours/day × 365.25 days/year =
31,557,600 seconds per year
• 100,000,000,000 ÷ 31,557,600 =
3168.8 years!
Structures of the Nervous System
I.
II.
III.
IV.
V.
Divisions of the Nervous System
Orienting within the Brain
The Developing Brain
The Adult Brain
Brain Plasticity
Anatomy Directions
(See figure 3.2, Page 65)
Anterior/Rostral
Posterior/Caudal
towards the head or front
towards the rear or behind
Ventral (Inferior)
Dorsal (Superior)
towards the belly (below)
Medial
close to the neuraxis
towards the back (above)
Lateral
away from the neuraxis
Ipsilateral
Contralateral
on the same side
on the opposite side
Convolutions of the Cortex
• Bump or ridge = gyrus (plural is gyri)
• Groove = sulcus (plural is sulci)
• Big groove = fissure
Receptors at the Synapse
• Receptor: Protein molecule embedded in a
membrane that has a binding site for one
or more neurotransmitters
– The binding site is like a key slot
– Neurotransmitter is like the key
Ionotropic Receptor
• Receptor contains an ion channel (or door)
that opens or closes when
neurotransmitter (NT) attaches to its
binding site
• Example: door to your house (ionotropic
receptor) has a key slot (binding site on
the receptor) that opens when you put in
and turn the key (neurotransmitter)
Metabotropic Receptor
• Receptor doesn’t contain an ion channel
• When Neurotransmitter attaches to
binding site, a G-protein changes
• Altered G-protein can affect near by ion
channels or activate “second messengers”
• Second messengers: 1) affect near by ion
channels and/or 2) activate DNA to
perform other cellular functions
Metabotropic Receptor Example
• Putting a key (neurotransmitter) into a key
slot (binding site on the receptor) causes a
near by elevator to turn on and open it’s
doors (G-protein or second messenger
opens near by ion channel) and sends a
message that the elevator is operating to a
control center elsewhere in the building
(G-protein affects other cellular processes)
Psychopharmacology
I. Introduction
II. Principles of Psychopharmacology
III. Sites of Action
Psychopharmacology
• The study of how drugs effect the nervous
system and behavior.
• Drugs have…
– effects: changes in behavior and/or
physiology
– sites of action: place in the body where the
drug interacts with the cells, causing some
kind of change
Pharmacokinetics
• Pharmacokinetics: The study of how drugs
are…
– absorbed
– distributed within the body
– metabolized (used) and
– excreted (gotten rid of)
Factors Influencing Drug Effects
• Route of administration
– Ingested vs. smoked vs. injected (Figure 4.1)
• Solubility
– Water soluble molecules can’t cross the BBB
– Lipid (or fat) soluble molecules can cross BBB
– Heroin more soluble in fat than morphine
– Given equal initial doses, more heroin gets to
the brain than morphine
Agonist
• Drug that facilitates or enhances the effect
of a neurotransmitter
– Nicotine is an ACh agonist
– Cocaine and amphetamines are dopamine
agonists
Antagonist
• Drug that counter-acts the effect of a
neurotransmitter
– 1st schizophrenia meds dopamine antagonists
– Botulinum toxin (botulism) is an ACh
antagonist
Tolerance
• Refers to how with repeated use of a drug,
it takes more of it to achieve the same
effect.
– Receptors on postsynaptic membrane may
disappear in response to repeated cocaine
use (cellular tolerance)
– With repeated consumption, more enzymes
are present in liver and blood to break down
alcohol, thus less gets to cells (metabolic
tolerance)
Tolerance Effects
• 100 milligrams of morphine typically
causes profound sedation and even death
in first time users
• Users with morphine tolerance have been
known to consume 4000 milligrams (40
times more) without adverse effects
• Amphetamine users can consume up to
100 times initial dose with tolerance
Withdrawal
• Symptoms opposite to those of a drug that
occur when someone stops taking a drug
that they have been using repeatedly.
• For example, if drug makes you happy and
euphoric, withdrawal symptoms may make
you depressed and down
Sensitization
• Refers to how with repeated use of a drug,
it takes less of it to achieve the same
effect.
• Less common than tolerance
• Thought to occur in response to
occasional or infrequent use
Would it help or hinder the effect of
a neurotransmitter if you…
1. Added more of the material needed to make
the neurotransmitter?
2. Interfered with the process of creating NT?
3. Prevented the NT from being stored in the
vesicles?
4. Tricked the vesicles into releasing NT (without
an action potential)?
5. Prevented calcium from triggering the release
of NT from the vesicles?
Would it help or hinder the effect of
a neurotransmitter if you…
6. Artificially activated a binding site of a
receptor?
7. Blocked the binding site of a receptor?
8. Artificially activated an autoreceptor?
9. Blocked an autoreceptor so that it
couldn’t detect neurotransmitter?
10. Prevented reuptake from happening?
11. Prevented the destruction of ACh?
Vision
I.
II.
III.
IV.
V.
Introduction
Nature of Light
Anatomy of the Visual System
Coding of Visual Information in the
Retina
Analysis of Visual Information
Sleep and Biological Rhythms
I.
II.
III.
IV.
V.
VI.
VII.
Introduction
Measuring Sleep
Stages of Wakefulness and Sleep
Why Do We Sleep?
Physiological Mechanisms of Sleep
Biological Clocks
Sleep Disorders
Neurotransmitters Involved in Arousal
Norepinephrine
Locus coeruleous (pons)
Acetylcholine
Basal forebrain and reticular
formation (in pons and
medulla)
Raphe nuclei (pons and
medulla)
Serotonin
Histamine
Tuberomammillary nucleus
(hypothalamus)
Hypocretin
Hypothalamus
Neural Control of Slow-Wave Sleep
• Ventrolateral preoptic area (basal
forebrain, in front of the hypothalamus)
• Destruction produces insomnia, coma, &
death
• Injection of adenosine into the basal
forebrain produces sleep
Neural Control of REM Sleep
• Peribrachial Area (in dorsolateral pons)
• Medial Pontine Reticular Formation
(MPRF)
– Remember reticular formation also involved in
alertness
• Damage to either area eliminates REM
sleep
Reproductive Behavior
I. Sexual Development
II. Hormonal Control of Sexual Behavior
III. Neural Control of Sexual Behavior
Gametes
• Almost all cells of the human body contain
23 pairs of chromosomes (46 Total) in their
nuclei
• Gametes (sperm and ova) have 23
individual chromosomes in their nuclei (23
Total)
Organizational Effects
• Hormone effect that directly changes
tissue differentiation and/or development
• Causes changes in structures of the
organism
• Organizational effects occur early in
development
• Not reversible
Activational Effects
• Effect of a hormone on the fully developed
(or mature) organism
• Act on pre existing structures, causing
some type of change
• Activational effects often depend on prior
organizational effects
• Examples: changes to boys and girls with
puberty, ovulation in women
Primordial Gonads
(bipotential or bisexual)
Genetic Females (XX) Genetic Males (XY)
No SRY gene SRY gene makes testis
determining factor
Gonads become ovaries
Gonads become testes
No testicular hormones
Testicular hormones
(anti-Müllerian hormone &
androgens)




Müllerian System
Develops
(feminization)
Wolffian System
Withers
(demasculinization)
Müllerian System
Withers
(defeminization)
Wolffian System
Develops
(masculinization)
Activational Effects of Sex Hormones at Puberty
(See Figure 9.5 in Text)
HYPOTHALAMUS
secretes: GnRH (Gonadotropin Releasing Hormone)

ANTERIOR PITUITARY
secretes: gonadotropic hormones (FSH & LH)

GONADS
Secrete: sex steroids

OVARIES
Secrete: estradiol (some testosterone)
TESTES
Secrete: testosterone (some estradiol)


hips widen, breast develop, and other
changes
facial hair, voice drops, and other changes
Ingestive Behavior
I.
II.
III.
IV.
V.
VI.
Physiological Regulatory Mechanisms
Drinking and Thirst
Eating and Metabolism
Signals that Start a Meal
Signals that Stop a Meal
Brain Areas Involved in Eating
Learning & Memory
I.
II.
III.
IV.
V.
Nature of Learning
Learning and Synaptic Plasticity
Perceptual Learning
Stimulus-Response Learning
Relational Learning
Definitions of Learning
• Psych 100:
– A relatively long lasting change in behavior or
potential behavior that is due to experience.
• This Class:
– The process by which experience changes
our nervous system and ultimately our
behavior.
The Hebb Rule
•
A synapse will be strengthened (more
easily activated and/or produce larger
depolarizations) if…
1. a synapse is repeatedly active when…
2. the post-synaptic neuron is firing.
Long-Term Potentiation (LTP)
• Defined: A long-term increase in the
excitability of a neuron to a particular
synaptic input caused by repeated highfrequency activation of that input.
• Though found to occur in numerous brain
areas, LTP was initially demonstrated in
the hippocampal formation
• Useful information: The entorhinal cortex
is the gateway to the hippocampus
A
B
C
Target
A
B
A
C
B
A
D
Object-Memory Task
(inferior temporal lobe
more active)
B
A
C
B
C
Spatial-Memory Task
(parietal lobe more
active)
Opiates
• Examples: morphine, heroin, codeine,
methadone
• Effect (site of action)
– Analgesia (periaquaductal gray matter)
– Hypothermia (preoptic area)
– Sedation (reticular formation)
– Reinforcement (mesolimbic system and
nucleus accumbens)
Addictive Behaviors and Classical
Conditioning
Drug (UCS)
Compensatory
response (UCR)
Drug paraphernalia
& environment (CS)
Compensatory
response (CR)
Many fatal drug overdoses occur when the
person uses in a non-familiar environment.
Why?
Alcohol & the NMDA Receptor
• Alcohol is an indirect antagonist of the
NMDA receptor
• Alcohol impairs LTP
• Other NMDA antagonist drugs…
– produce sedative effects
– produce anxiety reducing effects
– stimulate the release of DA in the nucleus
accumbens
Alcohol & the GABAA Receptor
• Indirect agonist for the GABAA receptor
• With alcohol, more inhibitory potentials are
created and thus more neurons are
hyperpolarized
• Drug Ro-15-4513 blocks this binding site
for alcohol on the GABAA receptor
• Impairment of GABAA receptors in the
cerebellum disrupts balance and
coordination
Integrating Schizophrenia Theories
• PFC is underactive (hypofrontality), perhaps
because of abnormal brain development,
negative symptoms produced
• PFC fails to excite DA neurons in the midbrain
• Underactive DA neurons in the midbrain create
further underactity in the PFC; more negative
symptoms are produced
• PFC fails to inhibit the release of dopamine in
the nucleus accumbens, making this area
overactive; positive symptoms are produced