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BIOBASES FINAL EXAM STUDY GUIDE
Topics/Cues
Genderal Nervous
System Structure
 CNS
 PNS
 SNS
 ANS
 P-SyNS
 SyNS
General Nervous
System Organization
 wrapping
 dorsal vs. ventral
Gray and white
matter
Major Brain
Landmarks (6)
Major Brain Lobes
(4)
Imaging Modalities
and Uses (7)
Nervous System
Development
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Divisions and Subdivisions
Central Nervous System
 Brain, spinal cord
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Peripheral Nervous System
 Divisions:
 Somatic Nervous System:
 receives sensory information from periphery
 conscious control of muscles
 WILLFUL or CONSCIOUS aspects of movement/sensation
 Autonomic Nervous System:
 UNCONSCIOUS aspects of movement/sensation of organs (e.g.,
heart, lungs, etc.)
 Divisions:
 Parasympathetic Nervous System: mostly inhibitory –
homeostasis
 Sympathetic Nervous System: excitatory – fight or flight
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From Periphery  Central
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neurons wrapped in myelin – endoneurium
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groups of neurons (fasicles) wrapped in perinuerium
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groups of fasicles and blood vessles (nerve) wrapped in epineurium
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Afferent nerves meet at Dorsal root ganglion
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From Central  Periphery
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Efferent nevers have their somas at the spinal cord on ventral side
Gray matter is the cell bodies; found on surface or cortex and center of spinal cord.
White matter is b/c of myelin—axons of neurons (send info); inside cortex and on
outside of spinal cord.
 Central sulcus: divides brain in half from anterior to posterior.
 Pre-central gyrus: anterior to central sulcus  primary motor cortex
 Post-central gyrus: posterior to central sulcus  somatosensory cortex
 Longitudinal fissure: seperates brain hemisphers
 Lateral fissure: seperates temporal lobe from frontal cortex
 Parietal-Occipital sulcus (internal): seperates occipital lobe from parietal lobe
 Frontal lobe: organization, planning, thinking
 Temporal lobe: memory, hearing
 Parietal lobe: association area
 Occipital lobe: visual processing
 X-ray: good for structural (i.e., bone) imaging  can damage cells; projection
 CT: use X-rays for structural imaging; not projection  rotate x-ray around head
 MRI: use mag rays for structural imaging; clear definition of white/gray matter
 PET: use radiation for functional imaging: projection; need time for radioactive
material to collect in area of brain of interest.
 SPECT: functional: cheap version of PET
 fMRI: images of increase O2 flow; functional and structural: not projection
 DTMRI: used to track motion of fluid in brain (how nerve travels in space)
 Embryonic Phase:
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 phases
(embryonic,
infant)
 piaget’s stages
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Cortex Development
Development
Pathologies
 4 types, 11
total disorders
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Pervasive Disorders
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Pituitary Hormones
(8)
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o simple mitosis until ~32 cells; then, specialization begins
o Day 15 = formation of neural streak in ectoderm
o Day 22 = neural tube forms
o Day 25 = neural tube closes
o Day 28 = 3 swellings form: prosen-. mesen-, and rhombencephalon
o etc….
o Mylenation isn’t completed until puberty
Infant phase:
o 9 – 10 months: motor neuron mylenation
o 2 – 4 years: occipital lobe fully develops
o 5 – 6 years: lateralization completes, plasticity lessened
o 12 – 16 year: frontal lobe fully develops
Piaget:
o Sensorimotor, 0 – 2 years: object perm., lang., myelin of vis., sense, motor;
frontal lobe density incr.
o Preoperational, 2 – 7: mental rep. of objects; words/pics to express;
lateralization completes
o Concrete Operational, 7 – 11: logical think; frontal lobe keeps develpng
o Formal Operational, 11+: abstract thinking; frntl lobe close to mature
develops from inside – out
neural precursors divide near ventricles, then migrate to cortex via glial cells
chemo attractors and repellents guide path of neuroplasts
Dorsal Induction Pathologies: (3 – 4 weeks)
o non-closure of neural tube = death
o Spina Bifida: incomplete closure of inferior end of tube
o Anencephaly: “no brain” – no closure of tube at superior end
o Encephalomeningocele: pouch of CSF/water in brain coverings
o Hydrocephalus: extremely large ventricles (too much fluid)
Ventral Induction Pathologies: (5 – 6 weeks)
o Holoprosencephaly: “the brain is one” – does not divide (cyclopia)
Proliferation Pathologies: (2 – 4 mn.)
o Micocephaly: “small brain” – smaller number of neurons
Migration Pathologies: (3 – 5 mn.)
o Agryria: “no gyri”; MR, seizures (less surface area for neurons)
o Pachygyria: “elephant gyri”; developmental delays
o Polymicrogyria: “many small gyri”; often due to uterine infection; MR,
seizures
o Heterotopia: homogenous white and gray matter; males = stillborn,
females = normal + seizures; less efficient processing
PDDs: compulsions, social, language
o Austistic: onset prior to age 3; genetic (MZ = 36 – 96%), brain diffs =
corpus collasum, frontal lobe, neural migration probs
o Asberger’s: normal or above avg intell; stereotyped bxs
o Rett’s: 5 – 48 months onset; decelerated head growth, loss of social
engagement; MR
o Child Disintegrative Disorder: loss of previously acquired skills by age 10
FSH – grow follicles
LH – ovulation
Prolactin – milk production
ACTH – adrenocorticotropic hormone; sends to adrenal glands to produce cortisol
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Sexual Development
Milestones
Arousal and
Consciousness
Circadian Rhythms
Motivation, Eating,
Addition
Relationships
Leptin
Mechanism of
Hunger/Satiety
Cannabinoid
Visual Pathway
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Growth hormone
TSH – thyroid stimulating hormone
Oxytocin – contractions, lactation, bonding
ADH – anti-diuretic hormone (blood volume)
6 Weeks:
o H-Y antigen in males causes gonads become testes
o lack of antigen in females; gonads become overares
 3 months:
o Testes  Mullerian inhibiting substance and androgens
o MIS  degeneration of mullerian ducts
o androgens  male organs
 Pathologies:
o Androgen Insensitivity Syndrome: no male sex organs (except testes b/c
of H-Y antigen) no mullerian tubes (b/c of MIS)
o Persistent Mullerian Duct Syndrome: mullerian tubes stay
 Reticular Activating System: nuclei in the pons, medulla, and brainstem
o locus coeruleous (novel stimuli)
o raphe nuclie (sleep)
o substantia nigra, ventral teg area (DA)
o cholinergenci basal forebrain  receives inputs from above nuclei and
projects to entire cortex
 SCN: suprachiasmic nuclei (over optic chiasm)
 uses genetic transcription to oscillate over a long time period
DA pathway in ventral teg and nucleus acumbens (increase of DA in nucleus
acumbens is necessary for natural reinforcers).
produced by fat tissues (adipose)  high levels increases metabolism, low levels
decrease metabolism
Too much fat:
 adipose  leptin
 leptin  hypothalamus (arcuate nucleus)  TSH and ACTH = increased
metabolism
 increased MSH  decreased feeding bxs
Too little fat:
 adipose  not enough leptin
 low leptin  hypothalamus (arcuate nucleus)  low TSH and ACTH = decreased
metabolism
 decreased orexin production = feeding bxs
Satiety:
 gastric dimension and nutrients
 intestinal nutrients
 liver senses glucose levels
 brain estimation of time delay
 INCREASED 5-HT = less eating
Receptors found in hypothalamus, limbic system, intestines, liver, adipose tissue,
pancrease
 Retina (with rods, cones, horizontal cells, bi-polar cells, ganglion cells)
 Optic Tract (optic chiasm) – splits and retinal hemisphers project to ipsilateral
LGN
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Primary Emotions
(6)
Secondary Emotions
Theories of Emotion
Fear (brain parts)
Agression
(types and parts)
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Facial Emotion
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Wernicke-Geschwind 
Model of Language
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(7 areas, functions,
deficits)
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Dual-Route Theory
and deficits
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Lateral Geniculate Nucleus (of thalamus)
Superior Colliculus (topographically mapped) – controls attention, head/eye move
Visual cortex
Definition: biologically based, innate; same for all humans
Joy, sadness, fear, disgust, surprise, anger
Sensory inputs go directly to limbic areas
Definition: dependent on learning and social environment
pride, shame, embarrassment, anxiety
Sensory inputs must first go to cortex and then to limbic areas
Frontal cortex is largely responsible
James – Lange: physiological changes  perceived emotion
Cannan – Bard: emotional experience can be independent of physiological changes
Cortex is not necessary
Amygdala: largely responsible for fear response  lesion = lack of fear response
Hypothalamus: hormone release b/c of fear
Predatory Agression:
o for killing; low SNS activation
o lateral HYPOTHALAMUS
Offensive Agression:
o emotional; high SNS activation
o medial HYPOTHALAMUS
AMYGDALA is CRITICAL
Left half of face is more expressive for SPONTANEOUS: right brain is where
emotional processing is concentrated
Right half of face is more expressive for POSED: left brain is where language is
processed.
Broca’s area: generates speech; deficit = problems creating speech, good RC
Primary motor cortex: sends commands to muscles of mouth for verbal speech, to
hand/arms for written.
Arcuate fasciculus: connects perceptive and productive areas of language. deficit =
problems in repetition – ok speak and RC.
Angular Gyrus: interpretation of visual language input. deficit = ok speech, no
reading, no writing.
Primary visual cortex: sensing visual information
Wernicke’s area: language comprehension (association of language inputs).
deficits = no comp, non-sensical speech, no semantics
Primary Auditory cortex: sense auditory language
Example: Response to heard question =
o audtory cortex  Wernicke’s area  arcuate fasciculus  broca’s area 
motor cortex
Received words are processed either through lexical or non-lexical processing
Lexical Route (temporal lobe):
o known and practiced words
o lexicon of known words located near WERNICKE’S AREA
o Deficit: left temporal lobe lesions = inability to pronounce words based on
specific memories i.e., well-known words
Non-Lexical Route (frontal lobe):
o uses rules of phonetics to interpret words
o rules surround BROCA’S area
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Memory Brain Areas
Lashley vs. Hebb
The Learning
Neurons
Long-Term
Potentation /
Depression
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Major Causes of
Brain Damage (8)
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Effects of Brain
Damage (3)
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CVAs how damage
Neuronal
Degeneration
Regeneration
(what will and what
won’t)
Plasticity
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o Deficit: left frontal lobe damage = inability to sound out new words
Short-term: right orbital cortex
Episodic / Spatial memory / Learning: hippocampus
Object recognition: rhinal cortex (adjacent to hippo)
Emotional Memory: Amygdala
Sensory Relay: Thalamus
Fornix / Mammillary Bodies: pathways in/out of hippo
Procedural: Striatum - CEREBELLUM
Lashley: thought memories were everywhere in the cortex
Hebb: proposed that when a neuron fires at the same time as a post-synaptic
neuron, the connection is strengthened.
Dendritic spine has NMDA receptors – need two keys, Glut and voltage. when
opened, allow influx of Ca++  second messenger  AMPA receptors & No2
AMPA receptors allow influx of Na+ (glutamate receptor)
LTP:
o Ca++ activates CaM-KII enzyme = controls synthesis of receptors,
phosphorylates the AMPA receptors, ps NO2
o spine / button splitting
o CREB-1 (phosphorylated) permits synthesis of AMPA receptors
LTD:
o AMPA receptors = dephosphorylated = less sensitive to glut
o AMPA receptors decrease in number, not replaced
o CREB is turned off
Genetic: faulty duplicatin of genes: Down’s, Turner’s, Klinefelter’s, Parkinsons,
etc. Usually self-limiting
Congenital: exposure to toxins, drugs, STDS, birth trauma
Environmental: radiation, toxins, drugs, nutrition
Neoplasms: aka cancer
Cell Death: aka necrosis – externally causes or apoptosis – normal
Cerebrovascular Problems: CVAs, Thrombosis – hypoxia = excess Ca++
Head Impact: trauma to brain – often damages area of brain opposite site of impact
Infections: syphillis, strep, rabies, herpes, mumps, etc.  inflammation of brain
(encephalitis) or meninges (meningitis)
Kill neurons: damage to nerve; damage to environment (e.g., glial cells); damage
to pre/post-synaptic nerves
Pressure: crowd out or place pressure on brain areas (e.g., neoplasms, meningitis,
encephalitis)
Diable neurons: myelin interference
Previous theory: lack of blood supply to designated neurons = death
Current theory: hypoxic (lack of O2) conditions cause NMDA receptors to allow
Ca++ influx = fossilizing neuron – hippocampus especially affected.
phagocytosis: “to eat” cells
Anterograde: the distal segments die: swell, fragment in days
Retrograde: the proximal segments: might live, might die
CNS: almost non-existent  growth inhibiting factors high in CNS
PNS: hit-or-miss  higher growth promoting factors
o if myelin sheath still intact, more likely to reconnect
o surrounding neurons may take place of dying axon (collateral sprouting)
Ability of neurons to reorganize: brain can remap its functioning; more likely in
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how does it work?
Pharmacology terms
 suffixes
 kinetics
 actions
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Schizophrenia –
Anatomical changes
(4 + 1 comment)
Theories of Schizo
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Anxiety Disorders
(the circuit and
pharmacology)
Affective Disorders
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younger
Rapid: short-term  altered sensitivity of receptors
Gradual: long-term; new connections formed
Suffixes: PAM = benzodiazapine; AL = barbituate; CAINE = local anesthetic
Kinetics:
o Metabolism: breakdown of drug by the liver; varies person to person
o Elimination: removal of drug by kidneys
o Half-life: time required to eliminate half of drug
Actions:
o availability of neurotransmitter (NT)
o release of NT
o block reuptake of NT
o alter autoregulation
o alter synaptic NT (breakdown in synapse)
o alter post-synaptic receptors (up/down reg.  2 – 3 weeks)
small cortex
large ventricles
prefrontal cortex and amygdala abnormal
smaller hippocampus
no ongoing degerneration (seems to already be in place at onset)
Dopamine Theory (Primary):
o increase DA in mesolimbic path (ventral teg to limbic (amygdala,
nucleus acumbens, hypothalamus)  positive symptoms
o decreased DA in mesocortical path  negative symptoms
Glutamate Theory:
o Glutamate controls inhibition in mesolimbic DA system
o Glutamate controls excitation in mesocortical DA system
o Lack of glutamate = increase emotional/fear, decrease thinking, logic
Other Factors:
o pre-natal stress increases risk
o pre-natal infections increases risk
o stressful precursor prior to onset is common
Senses & Thoughts  excite amygdala
amygdala  excites HPA (hypothalamus, pituitary, adrenal)
HPA  cortisol  excites hippocamus
hippocampus  inhibits HPA
5-HT increases hippocampal suppression of HPA
ANXIOUS PERSONS HAVE TOO LITTLE INHIBITION = not enough 5-HT
and not enough GABA
treat by increasing 5-HT in synapse (SSRIs) or increase GABA (e.g., valium)
Too much D, NE, 5-HT  MANIA
Too little “”  DEPRESSION
Pharmacology:
o MAOIs: keep enzymes from breaking down monamines = more
o TCAs: blocks reuptake of 5-HT and NE (safer)
o SSRIs: block 5-HT reuptake
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