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Neurobio > unit 4 > Flashcards

unit 4 Flashcards

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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
in heterosynaptic facilitation what activates transcription factors
PKA and C
25
long term potentiation (LTP)
used in fear conditioning; dependent of NMDA activation --> Na+ influx
26
what does LTP result in
an increased (potentiated) post-synaptic response to a given pre-synaptic stim
27
with LTP you can see an
increased EPSP in strengthen neuron
28
tone stim -->
goes to auditory thalamus and cortex; right before shock --> tone elicits fear response
29
how does the shock activate the amygdala
STRONGLY
30
how does the tone activate the amygdala ORIGINALLY
WEAKLY
31
lateral amygdala
input goes here
32
central amygdala
elicits fear response
33
via LTP tone goes from ____ to ____
weak signal to strong signal
34
fear response
lateral hypothalamus (LH) = increased heart rate; PVN = increased stress levels via HPA and cortisol; and freezing behavior
35
cellular mechanism for short-term
strengthening connection
36
in cellular mechanism for short-term LTP auditory and somatosensation neurons send
GLUT signal to LA
37
auditory has ____ receptors that do ____
AMPA --> Na+ influx
38
somatosensory has ___ receptors that do _____
NMDA --> Na+ and Ca2+ influx --> increase CAMK --> PO4 AMPA --> increased number of AMPA receptors
39
what transcription factor is critical for cellular mechanism for long term LTP
CREB
40
what are neuropsych disorders
disorders of brain connectivity
41
how do neuropsych disorders work
stimuli thru repeated exposure lead to new behavioral response
42
why is associative learning important
because it has implications for understanding behavior both in "normal" and pathogical context
43
what plays a role in anxiety disorders
dysregulation of the fear response is thought to
44
what are the symptoms of the fear response
freeing, increased blood pressure, secretion of stress hormones
45
fear conditioning - anxiety
cued fear conditioning (amygdala dependent) and contextual fear conditioning (hippocampus)
46
fear extinction learning
occurs when repeated presentation of a stim (S) no longer predicts an aversive outcome (US) to a gradual decrease in learned fear responses
47
why is fear extinction not "erasing" fear conditioning
not "erasing" fear association but forming a new association that competes with fear condition
48
medial prefrontal cortex (mPFC)
key regulator of fear response/extinction - thought to inhibit conditioned responses following extinction
49
how does mPFC inhibit conditioned responses following extinction
subdivision of mPFC (IL) acts on ITC cells in amygdala to inhibit expression of fear by the central amygdala following extinction
50
what power does PFC have over other parts of the brain
PFC (cortex) "controls" subcortical regions (amygdala, hippocampus, etc) as PFC is "rational brain"
51
hypofrontality
PFC can't "control" subcortical regions/can't stop them - no impulse control
52
CBT
most effective evidence-based psych treatment for anxiety disorders
53
exposure therapy
gradually exposing individual to feared stim/outcome in absence of danger - prevent conditioned fear
54
A-B-A renewal
fear conditioning - extinction learning - fear response to CS - can bring back fear
55
operant conditioning
drug acts as instrumental reinforcers by activating reward pathway circuits in brain
56
animals an learn to press leer to deliver stim to stimulate pathway
MEANING both days of abuse and activation mesocorticolimbic circuity have this reinforcing effect
57
operant and contextual/classical conditioning - drug abuse
an occur at same time and can both elicit feelings of pleasure
58
operant and contextual/classical conditioning MEANING
stim associated with drug cues an elicit responses and become associated with reinforcing outcome related to taking the drug itself
59
cue reactivity treatment
showing stim and trying to weaken association to subjective pleasure.
60
mesocorticolimbic pathway
"pleasure pathway" - VTA (midbrain) -- sends dopamine --> to NAc = pleasure
61
all drugs of abuse impact
mesocorticolimbic pathway (drugs not associated with abuse don't)
62
"reward" =
subjective high/pleasure
63
conditioned compensatory response
drug cue conditioned stim an elicit this; creates opposite response to drug before taking it; essentially "prepping" body for said drug
64
can build up ____ due to conditioned compensatory response
tolerance
65
if see drug cue conditioned stim and don't take drug
withdrawal symptoms
66
if take drug and no cue conditioned stim = no conditioned compensatory responses =
overdose
67
why might overdose happen
because body wasn't "prepped" and therefore couldn't handle as uh as it could have if conditioned compensatory responses
68
initially a particular response/behavior is controlled by
valuation of given outcome = goal-directed drug seeking
69
goal-directed can become less important with a learning shift -->
drug related stim elicits a compulsive habitual response

Neurobio (6 decks)

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