Biopsych Test 2 Spitzer

Front 1

6 Steps of Nervous System Development

Back 1

1. Proliferation – the production of new cells
2. Migration – after cells have differentiated as neurons or glia they migrate depending upon chemicals that guide immature neurons
3. Differentiation - formation of the axon and dendrites that gives a neuron its distinctive shape
4. Synaptogenesis - formation of synapses
5. Apoptosis – when a neuron kills itself at a certain age unless inhibited from doing so
6. Remodeling

Front 2

→ 21 days post-conception: the neural plate (ectoderm)

Back 2

--forms the neural tube
--central cerebral ventricles
(the CNS (brain and spinal cord) begins as a tube surrounding a fluid filled cavity at 2-3 weeks)

Front 3

→ 40 days

Back 3

3 swellings (forebrain, midbrain, hindbrain)

Front 4

proliferation

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--ventricular zone for neurons, early
--normal neonatal brain has 2-3x the required number of n.

Front 5

stem cells

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undifferentiated cells that can divide and produce daughter cells that develop more specialized properties

a. totipotent cells = stem cells
b. pluripotent = stem cells further along in development
c. progenitors = further developmental restriction (ex: ‘glia’)

Front 6

proliferation errors

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anencephalus (parts of brain/ skull missing at birth)

Front 7

migration

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movement of neurons toward their eventual destinations in the brain

--radial glia
--inside-out pattern in 6 layered cortex
--chemoattractants (induces a cell to migrate toward it); chemorepellants (repel)
--aggregation by cell adhesion molecules (CAMs) – (proteins located on the cell surface involved with the binding with other cells)

Front 8

migration errors

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mental retardation

Front 9

differentiation

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formation of the axon and dendrites that gives a neuron its distinctive shape

--polarity established; axon growth (axons grow before dendrites)
--growth cones with filopodia and lamellipodia

Front 10

chemoaffinity hypothesis

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(neurons make connections with their targets based on interactions with specific molecular markers)

Front 11

Sperry 1940s

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target-derived factors (NTF/GFs) – after he cut the optic nerve and inverted the eye, the optic nerve axons grew back to the original targets, not to the targets corresponding to the eye’s current position

Front 12

synaptogenesis

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formation of synapses

--growth factors/neurotrophins (trophic = to nourish)
--functional synapses
--prenatal spontaneous action potentials in retinal ganglion cells
---thalamus receives inputs from retinas and selects activated neurons

Front 13

apoptosis vs. necrosis

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apoptosis - a neuron kills itself at a certain age unless inhibited from doing so

necrosis – death caused by an injury or a toxic substance

Front 14

necrosis errors

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cancer, neurodegeneration

Front 15

remodeling

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a. pruning from diffuse connectivity to focused
---sensory cortex at 4 mo; prefrontal at 2 yr (object permanence)
--adolescence second growth spurt
b. dendritic sprouting the most plastic process throughout life; hippocampus
c. myelination sensory systems in mos., prefrontal cortex in years

Front 16

Effects of Environment on Development

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--use it or lose it
--neural Darwinism
--competitive nature
---deprivation studies; visual

Front 17

How could experience influence biology and therefore neurodevelopment?

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neural activity → release of neurotrophins in dendrites
neurotrophins = neurotrophic factors = growth factors

Front 18

Fine-tuning by experience = Plasticity

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--activation = preservation
---dendritic branching, reorganization of cortical maps
--plasticity decreases with age

Front 19

Vulnerability to Injury

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--periods of extreme vulnerability
1. during fetal development
2. during two postnatal critical periods
---first 3-5 years
---mid-teens to early twenties
3. during aging

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Types of Insults

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1. genetic mutations
2. chemicals (FAS)
3. malnutrition
4. infections; bacterial, viral
5. injury

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fetal alcohol syndrome (FAS) effects

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---decreased alertness, hyperactivity, mental retardation, motor dysfunction, heart defects, facial abnormalities
---as adults at risk for alcoholism, drug dependence, depression, other psychiatric disorders

Front 22

stroke

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temporary loss of normal blood flow to a brain area

sudden onset vascular events; infarcts; 3rd cause of death; coma, paralysis, aphasia, amnesia

Front 23

types of strokes

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1. ischemia = disruption of blood supply resulting in lack of oxygen (anoxia - lack of oxygen) ex. blood clot

2. hemorrhage = blood vessel rupture; aneurysm (congenital, toxins/poisons, infection, high blood pressure)

Front 24

result of stroke

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- delayed secondary injury
- increasing penumbra

Front 25

Closed-head Injuries

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concussion = blow to the head, disruption of consciousness
--punch-drunk syndrome (boxers), dementia

Front 26

Neurotoxins - brain injuries

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Mad Hatter – mercury in hat felt

crackpot – tea seeped in lead-based ceramic glazes on teapots

Front 27

Degeneration

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Wallerian (retrograde)
anterograde
transneuronal degeneration
(The degeneration of a nerve fiber that has been separated from its nutritive center by injury or disease & axon dies)

Front 28

Secondary injury

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an indirect result of the injury (processes initiated by the trauma)
- occurs hours and days following the primary injury

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Apoptosis

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developmental program by which a neuron kills itself at a certain age unless inhibited from doing so

Front 30

Regeneration

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oligodendrocyte inhibitors
Schwann cell conduits

Front 31

Synapse formation and dendrite branching

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--practicing a skill can reorganize or restructure the adult brain

Front 32

Neurogenesis in adult mammals

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hippocampus – 2,000/hr
--adult rats living in an enriched environment produce 60% more than controls
association cortex also – numbers unknown

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Reorganization

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--sensory/motor cortex; visual system

Front 34

goals of treatment to injury

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1. reduce secondary injury
2. enhance regenerative effort of CNS

Front 35

types of treatments for brain injury

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1. corticosteroids (estrogens)
2. transplantation
stem cells
olfactory ensheathing cells
3. growth factors

Front 36

left-brained or right-brained supposedly:

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L = analytical, logical, verbal
R = creative, holistic, spatial

Front 37

Visual and auditory connections to the hemispheres

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--in prey animals, L eye to R hemisphere and R eye to L hemisphere
--in humans, partial decussation at optic chiasm
--auditory axons project to both hemispheres; contralateral (other side) is dominant

Front 38

Cutting the corpus callosum

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--Sperry and Gazzaniga 1960s
--intractable epilepsy; ‘split brain’ surgery

Front 39

Split hemispheres: competition and cooperation

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--clothing selection
--cueing the other hemisphere with a frown

Front 40

handedness

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most right handed people are L hemisphere dominant for language

Front 41

tests of lateralization

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1. sodium amytal (Wada)
2. imaging; PET, fMRI
3. split brain surgery (commissurotomy)
4. dichotic listening

Front 42

The right hemisphere

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--spatial relationships
--emotional content; gestures, facial expressions
--L hemisphere damage allows R to make reliable judgments (60% correct guessing if others were lying)

Front 43

L vs R (analytical vs holistic)

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L - analytic, more details
R - holistic, overall patterns
(letter H written with small B's)

Front 44

Hemispheric specialization in intact brains

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--small, subtle differences
(tapping your shoulders = most right hangers, talking decreases the tapping rate with the right hand = more difficult to do both things at once when both activities depend on the same hemisphere)

Front 45

Anatomical differences between the hemispheres

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---Geschwind and Levitsky
--speech comprehension (Wernicke’s area)
--planum termporale - area of the temporal cortex that for most people is larger in the left hemisphere than in the right hemisphere;
L larger in 65% people

Front 46

AVOIDING OVERSTATEMENTS

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1. the hemispheres are specialized for different functions
2. certain tasks evoke greater activity in one hemisphere or the other
3..no individual habitually relies on one hemisphere more than the other
--almost all tasks require cooperation between the hemispheres

Front 47

circadian

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rhythms that last about a day; waking/sleeping, eating and drinking, body temperature, hormone secretion, urination, drug sensitivity

Front 48

Biological Clock

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the endogenous (generated from within), physiological mechanism for controlling a behavior that recurs on a regular schedule
avg. - 24.3 hours

Front 49

Biological Clock - Age differences

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older people - wake and sleep earlier
young adults - later

Front 50

Neural Mechanisms of internal clock

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--the internal clock is relatively insensitive to changes in food, water; x-rays, tranquilizers, alcohol, anesthesia, lack of oxygen, most types of brain damage, removal of hormonal organs

Front 51

Suprachiasmatic Nucleus (SCN)

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area of the hypothalamus, located just above the optic chiasm, that constitutes the biological clock

--damage reduces consistency of rhythms, sensitivity to light changes
-- SCN neurons removed still demonstrate circadian rhythms (Even a single one); measure output of chemicals (APs????; transplants in hamsters – 20 – 24 hours, rhythm followed donors)

Front 52

How light resets the SCN?

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light alters production of proteins period (Per) and timeless (Tim) which act on protein clock in the SCN to produce sleep
high per and tim = sleepiness
low = wakefulness

Front 53

--axons of the retinohypothalamic path directly to SCN

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the retinohypothalamic path = small branch of the optic nerves from retina to SCN

Front 54

melanopsin

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-- retinal cells (not rods/cones)
-- respond to average amount of light (not sudden changes)

Front 55

Melatonin

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-- hormone that induces sleepiness
--melatonin receptors in the SCN
---taking melatonin can cause you to phase-advance (get sleepy) best in afternoon

Front 56

zeitgeber

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“time-giver” = environmental cues that entrain (control or change) circadian rhythms

Front 57

what is the strongest zeitgeber for land mammals?

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light!

--free-running experiments demonstrate circadian rhythms
---tendency to shift; zeitgebers are used to ‘reset’ clock

Front 58

Importance of light

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the rhythm is reset by bright light more effectively than high activity levels or body temperature; shift workers never fully adjust

Front 59

Jet Lag & phases

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= a disruption of biological rhythms due to crossing time zones
--going west you phase-delay the cycle (gain time) easier
--going east you phase-advance the cycle (lose time) harder

Front 60

polysomnogram

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combination of EEG and eyemovement records, and sometimes other data, for a sleeping person
(EEG, EMG or EOG)

Front 61

Sleep Stages

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- alpha waves (relaxed/ awake)
- stages 1 - 4
- REM

Front 62

polysomnogram levels

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a. alpha waves (8-12/sec) – relaxed, awake
b. stage 1 sleep = irregular, jagged, low-voltage waves
c. stage 2 sleep = sleep spindles, K complexes
d. stage 3 sleep = heart rate, breathing rate, brain activity slower than in previous stage, percent of slow, large- amplitude waves increases – Slow Wave Sleep
e. stage 4 = slow waves (neuronal activity is highly synchronized) – Slow Wave Sleep
f. REM = rapid eye movement sleep; PGO waves

Front 63

sleep cycles

Back 63

1. enter stage 1, slowly progress through 2, 3, 4 in order; stimuli can cause a reversal or awakening
2. 60-90 minutes later, cycle back from stage 4 to 3 and 2 and enter REM
3. cycle repeats; each approx. 60-90 min.
4. early in the night, stages 3 and 4 dominate
5. toward morning, stage 4 grows shorter; REM longer
1→2→3→4→3→2→REM→2→3→4→3→2→REM→etc.

Front 64

midbrain; reticular formation (RAS)

Back 64

midbrain; reticular formation (RAS) - network of neurons in the medulla and other parts of the brainstem;
the descending portion controls motor areas of the spinal cord;
the ascending portion selectively increases arousal and attention in various forebrain areas
---sensory input to thalamus, forebrain; glutamate and acetylcholine so excitatory inputs; from thalamus to cortex

Front 65

locus coeruleus

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(in pons) releases norepinephrine in bursts in response to meaningful events; target cells activate genes involved in memory
(during sleep, the LC is inactive - why we don’t remember our dreams?)

Front 66

hypothalamus influence arousal

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- releases histamine = excitatory effects
- releases orexin
- connects basal forebrain to thalamus, cortex axons release acetylcholine; GABA during sleep

Front 67

orexin

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(hypocretin) goes to forebrain and brainstem, stimulating ACh for staying awake

--narcolepsy - body doesnt release/ make orexin

Front 68

two strategies to help getting to sleep

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1. inhibit the arousal system!
--adenosine receptors in basal forebrain inhibit acetylcholine activity; adenosine levels increase during the day until sleep then decline
---caffeine inhibits adenosine (inhibit the inhibitor)
2. excite the inhibitor system!
--GABA axons from forebrain (BDZ)

Front 69

paradoxical sleep

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in some ways the deepest sleep in some ways the lightest (low-voltage, fast waves ); correlated with time of rapid eye movements

Front 70

REM sleep characterized by:

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1) irregular, low-voltage, fast waves suggesting considerable brain activity (light sleep)
2) postural muscles more relaxed than in any other stage
3) facial twitches, eye movements
4) a distinct pattern of high-amplitude electrical potentials; PGO waves synchronize with eye movements
=pons-geniculate (LGN of thalamus)-occipital
--pons inhibits motor neurons in spinal cord

Front 71

insomnia

Back 71

onset - difficulty falling asleep
maintenance - waking up frequently
termination - waking up early

Front 72

Other sleeping disorders

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2. sleep apnea = inability to breath while sleeping
3. narcolepsy (intrusion of REM sleep; orexin mutation)
4. periodic limb movement disorder; NREM
5. REM behavior disorder; vigorous movements during REM (associated with damage to what area?)
6. night terrors during NREM
7. sleep talking same during NREM and REM
8. sleepwalking during NREM
9. insomnia

Front 73

Hunger

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--evolutionary pressure is to actively eat, not to stop eating
--eating and satiety are a function of:
sight, smell, taste, learning, social factors, hunger

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satiety depends on

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1. volume of food
2. nutritive density (calories per volume)
3. social influences; alone or with others
4. sensory-specific; cafeteria diet
--the appetizer effect
---small amts of food premeal increase hunger
5. hunger

Front 75

anorexia (orexis = appetite)

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- secondary to illness, or anorexia nervosa
- refusal to eat
- begins in adolescence
- 90-95% are female; male numbers increasing
- report that they are not hungry
- social, environmental, genetic predisposition
- associated with elevated cortisol levels (depression)

Front 76

bulimia (morbid hunger)

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- alternate between dieting and overeating
- binging/purging
- extreme urges to eat, then guilt about eating
- mostly women
- eating associated with reinforcement (DA)
- decreased serotonin and serotonin receptors(depression)

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overweight

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- national health crisis
- overweight heritability ~ .4 to .7
- over ½ Americans are clinically obese
- increased risk factor for numerous health problems

Front 78

signals at every level of the eating process

Back 78

1. sight/smell – cortex and ANS; saliva, gastric secretion
2. mouth – chewing
3. stomach – gastric distension, vagus nerve
4. duodenum – CCK (satiety) sugar signals faster than fat
5. pancreas -- produces insulin and glucagon

Front 79

pancreas

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-- produces insulin and glucagon
a. insulin signals “storage;” it is a hormone that moves blood sugar into cells for storage
b. glucagon signals “release stored sugar;” causes the liver to convert stored glycogen (stored sugar) to glucose (usable sugar), raising blood glucose (sugar)

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After the Meal

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food is metabolized and stored as energy in two forms: glycogen and triglycerides

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glycogen

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---liver can only store 3-day’s worth of glycogen
---very little in skeletal muscle

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triglycerides

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(fat; unlimited capacity, long-term storage)
---fat cells are permanent

Front 83

1940s lesion studies

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---lesions to lateral hypothalamus LH = anorexia
---lesions to VMH = overeating
--resulted in calling the hypothalamus a ‘feeding center’ and ‘satiety center’
--too simplistic: actually several nuclei are involved in feeding behaviors; LH, VMH, PVN, arcuate

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1953 the lipostatic hypothesis – a body fat set point –

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communication between adipose tissue and the brain

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leptin

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peptide released by fat cells; tends to decrease eating, partly by inhibiting release of neuropeptide Y in the hypothalamus

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Arcuate nucleus

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hypothalamic area with one set of neurons sensitive to hunger signals and another sensitive to satiety signals & releases peptide NT depending on leptin levels

Front 87

two anorectic peptides used as NT by the arcuate nucleus

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1. αMSH (alpha melanocortin)
2. CART (cocaine and amphetamine regulated transcript)

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two orexigenic peptides used as NT by the arcuate nucleus

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1. NPY (neuropeptide Y)
2. AgRP (agouti-related protein)

Front 89

two orexigenic peptides used by the LH to signal cortex

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--decreased leptin? = arcuate n. signals cells in the LH which have diffuse projects to cortical areas that mediate organizing and initiating goal-directed behaviors, using:
1. MCH (melanin-concentrating hormone)
2. orexin/hypocretin