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Neurobio > unit 4 > Flashcards

unit 4 Flashcards

1
Q

what is thought to represent the cellular basis of memory

A

changes in synaptic strength/plasticity

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2
Q

what organism have researchers used to learn more about non-associative forms of memory

A

Aplysia California - with reflex pathways

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3
Q

habituation in terms of the sea slug

A

repetitive stimulation of siphon leads to decrease in gill withdrawal effects

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4
Q

monosynaptic depression

A

reduced NT (glutamate) release from sensory neuron (so motor neuron is less stimulated)

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5
Q

with habituation and monosynaptic depression of the sea slug

A

AP of the sensory neuron is unchanged
BUT
EPSP on motor neuron and gill withdrawal decreased

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6
Q

sensitization in terms of the sea slug

A

a shock is applied to the tail at the same time the touch stimulus is applied to the siphon, leading to increased gill withdrawal - above baseline

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7
Q

for sensitization with interneuron

A

interneuron releases serotonin onto axon terminal adn cell body

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8
Q

for habituation what NT does the siphon sensory neuron release onto the gill motor neuron

A

glutamate

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9
Q

for sensitization what NT does the tail sensory neuron release onto the siphon sensory neuron and where on the siphon sensory neuron

A

it releases serotonin onto the cell body and axon terminal

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10
Q

heterosynaptic facilitation cause

A

release of serotonin activates metabotropic receptors on siphon sensory neuron

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11
Q

what does heterosynaptic facilitation do

A

strengthens the connection between siphon sensory neuron and gill motor neuron

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12
Q

what do 5HT receptors impact

A

ion channels, kinases, and transcription factors

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13
Q

5HT

A

serotonin

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14
Q

pathway for Gas in cellular mechanism for short term facilitation

A

5HT binds to 5HT receptors –> Gas dissociates –> increased AC levels –> increased cAMP levels –> activates protein kinase A (PKA)

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15
Q

pathway for Gaq in cellular mechanism for short term facilitation

A

5HT binds to 5HT receptors –> Gaq dissociates –>increased DAG levels –> activates protein kinases C (PKC)

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16
Q

what happens in the cellular mechanism for short term facilitation when PKA and C are activated

A

phosphorylation (PO4) of K+ channels inhibiting them

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16
Q

what are leakage channels important for

A

resting potential (-70mV)

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17
Q

what K+ channels are inhibited with PO4

A

leakage channels and voltage-gated

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18
Q

what happens when K+ leakage channels are inhibited

A

less K+ leaking out; resting membrane potential will increase = AP is more likely to fire

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19
Q

what are VG K+ channels important for

A

falling phase of AP - hyperpolarization

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20
Q

what happens when VG K+ channels are inhibited

A

AP will last longer; more NT release

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21
Q

why is the cellular mechanism for short term facilitation not long-term

A

PO4 will get taken off

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22
Q

cellular mechanism for long-term facilitation

A

same thing with 5HTR but have to grow new connections between neurons

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23
Q

how are new connections between neurons grown

A

transcription factors are activated –> bind to DNA and alter gene expression (transcription) –> new proteins are synthized –> morphological/structural changes occur

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24
Q

in heterosynaptic facilitation what activates transcription factors

A

PKA and C

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25
Q

long term potentiation (LTP)

A

used in fear conditioning; dependent of NMDA activation –> Na+ influx

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26
Q

what does LTP result in

A

an increased (potentiated) post-synaptic response to a given pre-synaptic stim

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27
Q

with LTP you can see an

A

increased EPSP in strengthen neuron

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28
Q

tone stim –>

A

goes to auditory thalamus and cortex; right before shock –> tone elicits fear response

29
Q

how does the shock activate the amygdala

A

STRONGLY

30
Q

how does the tone activate the amygdala ORIGINALLY

A

WEAKLY

31
Q

lateral amygdala

A

input goes here

32
Q

central amygdala

A

elicits fear response

33
Q

via LTP tone goes from ____ to ____

A

weak signal to strong signal

34
Q

fear response

A

lateral hypothalamus (LH) = increased heart rate; PVN = increased stress levels via HPA and cortisol; and freezing behavior

35
Q

cellular mechanism for short-term

A

strengthening connection

36
Q

in cellular mechanism for short-term LTP auditory and somatosensation neurons send

A

GLUT signal to LA

37
Q

auditory has ____ receptors that do ____

A

AMPA –> Na+ influx

38
Q

somatosensory has ___ receptors that do _____

A

NMDA –> Na+ and Ca2+ influx –> increase CAMK –> PO4 AMPA –> increased number of AMPA receptors

39
Q

what transcription factor is critical for cellular mechanism for long term LTP

A

CREB

40
Q

what are neuropsych disorders

A

disorders of brain connectivity

41
Q

how do neuropsych disorders work

A

stimuli thru repeated exposure lead to new behavioral response

42
Q

why is associative learning important

A

because it has implications for understanding behavior both in “normal” and pathogical context

43
Q

what plays a role in anxiety disorders

A

dysregulation of the fear response is thought to

44
Q

what are the symptoms of the fear response

A

freeing, increased blood pressure, secretion of stress hormones

45
Q

fear conditioning - anxiety

A

cued fear conditioning (amygdala dependent) and contextual fear conditioning (hippocampus)

46
Q

fear extinction learning

A

occurs when repeated presentation of a stim (S) no longer predicts an aversive outcome (US) to a gradual decrease in learned fear responses

47
Q

why is fear extinction not “erasing” fear conditioning

A

not “erasing” fear association but forming a new association that competes with fear condition

48
Q

medial prefrontal cortex (mPFC)

A

key regulator of fear response/extinction - thought to inhibit conditioned responses following extinction

49
Q

how does mPFC inhibit conditioned responses following extinction

A

subdivision of mPFC (IL) acts on ITC cells in amygdala to inhibit expression of fear by the central amygdala following extinction

50
Q

what power does PFC have over other parts of the brain

A

PFC (cortex) “controls” subcortical regions (amygdala, hippocampus, etc) as PFC is “rational brain”

51
Q

hypofrontality

A

PFC can’t “control” subcortical regions/can’t stop them - no impulse control

52
Q

CBT

A

most effective evidence-based psych treatment for anxiety disorders

53
Q

exposure therapy

A

gradually exposing individual to feared stim/outcome in absence of danger - prevent conditioned fear

54
Q

A-B-A renewal

A

fear conditioning - extinction learning - fear response to CS - can bring back fear

55
Q

operant conditioning

A

drug acts as instrumental reinforcers by activating reward pathway circuits in brain

56
Q

animals an learn to press leer to deliver stim to stimulate pathway

A

MEANING both days of abuse and activation mesocorticolimbic circuity have this reinforcing effect

57
Q

operant and contextual/classical conditioning - drug abuse

A

an occur at same time and can both elicit feelings of pleasure

58
Q

operant and contextual/classical conditioning MEANING

A

stim associated with drug cues an elicit responses and become associated with reinforcing outcome related to taking the drug itself

59
Q

cue reactivity treatment

A

showing stim and trying to weaken association to subjective pleasure.

60
Q

mesocorticolimbic pathway

A

“pleasure pathway” - VTA (midbrain) – sends dopamine –> to NAc = pleasure

61
Q

all drugs of abuse impact

A

mesocorticolimbic pathway (drugs not associated with abuse don’t)

62
Q

“reward” =

A

subjective high/pleasure

63
Q

conditioned compensatory response

A

drug cue conditioned stim an elicit this; creates opposite response to drug before taking it; essentially “prepping” body for said drug

64
Q

can build up ____ due to conditioned compensatory response

A

tolerance

65
Q

if see drug cue conditioned stim and don’t take drug

A

withdrawal symptoms

66
Q

if take drug and no cue conditioned stim = no conditioned compensatory responses =

A

overdose

67
Q

why might overdose happen

A

because body wasn’t “prepped” and therefore couldn’t handle as uh as it could have if conditioned compensatory responses

68
Q

initially a particular response/behavior is controlled by

A

valuation of given outcome = goal-directed drug seeking

69
Q

goal-directed can become less important with a learning shift –>

A

drug related stim elicits a compulsive habitual response

Neurobio (6 decks)

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