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PSYC 318 > Midterm 2 > Flashcards

Midterm 2 Flashcards

(47 cards)

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1
Q

Synaptic strength formula

A

M = NPQ

where:
- N = number of synapses (pre-synaptic)
- P = probability of vesicles being released (pre-synaptic)
- Q = Amplitude of PSP following single vesicle release (mainly post-synaptic)

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2
Q

Ways to change P in M = NPQ

A
  • increase Ca2+ channels at axon terminal
  • increase # of vesicles ready to be released
  • coupling Ca2+ entry with fusion of vesicles
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3
Q

Signaling cascade causing STF in aplysia model

A
  1. 5HT (serotonin) binds to GPCR, a metabotropic receptor, releasing G proteins
  2. G proteins activate adenylyl cyclase
  3. Adenylyl cyclase creates cyclic AMP (cAMP)
  4. cAMP activates PKA
  5. PKA phosphorylates K+ channels
  6. K+ channels close or less effective -> longer depolarization -> more Ca2+ can enter -> more nrtrm release
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4
Q

Ways to increase Q in M = NPQ

A
  • change amount of nrtrm in vesicle (pre-synaptic)
  • change # / efficacy of post-synaptic receptors
  • change ion concentration (post-synaptic)
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5
Q

Associative proteins

A
  • proteins that sense pairing of CS and US
  • “coincidence detectors”
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6
Q

Signaling cascade driving LTP in hippocampal CA1-CA3

A
  1. depolarization (through AMPA receptors) + glutamate binding opens up NMDA receptors
  2. Ca2+ ions enter cell through NMDARs -> signaling cascade activates CAMKII and PKC (which are kinases)
  3. phosphorylation of unknown protein drives exocytosis of AMPA receptors on post-synaptic density
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7
Q

Purkinje neuron inputs and outputs

A
  • in cerebellar cortex

Inputs:
- CS (air puff) input from inferior olive
- US input from auditory pathway (pontine nucleus)

Ouputs:
- inhibitory outputs to interpositus nucleus which drives associative learning

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8
Q

LTD mechanisms in cerebellum Purkinje neurons

A
  1. depolarization + glutamate binding (US + CS) -> Ca2+ entry
  2. Ca2+ dependent signaling cascade -> activates PKC alpha
  3. PKC alpha phospohrylates AMPARs, reducing binding of GRIP
  4. GRIP not here, so PICK comes around -> endocytosis of AMPARs
  5. fewer AMPARs -> smaller EPSP; LTD
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9
Q

GluA2 receptors

A
  • isoform of AMPARs
  • last 4 amino acid are SerineLKI
  • GRIP binds to serine
  • PKC alpha phosphorylates Serine -> prevents GRIP binding
  • however, PICK binds to I of GluA2 so it can now take away GluA2
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10
Q

3 roles of phosphorylation

A
  • adds negative charge leading to conformational change
  • creates binding site for protein-protein interaction; e.g. a certain protein only binds to phosphorylated serine, tyrosine or threonine
  • destroys binding site for protein-protein interaction; e.g. a certain protein only binds to unphosphorylated serine, tyrosine or threonine
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11
Q

Possible mutations to study role of phosphorylation what they would mean for the 3 roles of phosphorylation

A

Serine -> alanine mutation
1. adds positive charge so blocks conformational change, blocks phosphorylation

Serine -> glutamic acid mutation
1. adds negative charge so mimics conformational change, mimics phosphorylation

  1. if phosphorylation effect is binding site creation, then these mutations will not be able to be phosphorylated -> will block binding site creation -> block phosphorylation
  2. if phosphorylation effect is binding site destruction, then both of these mutations change molecule and destroy binding site-> will mimic phosphorylation
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12
Q

Role of phosphorylation of GluA2 in LTD

A
  • destroys serine binding site
  • GRIP binds to serine and unbinds when phosphate group comes around
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13
Q

Mutating lysine to _________ in GluA2 receptors __________ phosphorylation of ____________ by ____ and therefore blocks ____

A

alanine, blocks, serine, PKC alpha, LTD

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14
Q

Eyeblink response to LTD blocking

A
  • unaffected
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15
Q

How does CREB work?

A

CREB is a protein that binds to a gene promoter called CRE which drives transcription of PRPs in the presence of cAMP -> allowing LTP to occur

Three key events for CREB to drive transcription:
- homodimerization, as opposed to CREB-CREB repressor dimerization which prevents gene transcription
- phosphorylation so that CBP can bind
- CBP binding and therefore activating CREB homodimer ability to transcribe

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16
Q

How is 5HT released during sensitization vs habituation?

A

sensitization:
- released by adjacent tail sensory neuron during e-shock

habituation:
- not released during habituation

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17
Q

Kir2.1

A
  • K+ channel that pushes K+ out of cell
  • lowers resting potential -> less excitable
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18
Q

Role of DNA methylation in memory

A
  • downregulates transcription of PRPs transcription inhibitors
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19
Q

dnKCNQ2

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A
  • K+ channel that allows less K+ to leave cell during refractory period -> no overhyperpolarization -> easier to firing beyond threshold after AP
  • dn stands for dominant negative, acts as a heterodimer -> inactivates its endogenous K+ channels
  • upregulates a cell’s excitability
20
Q

Which amino acids can be phosphorylated?

Study These Flashcards
A
  • serine (S)
  • threonine (T)
  • tyrosine (Y)
21
Q

How was LTD blocked in mouse model?

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A
  • lysine gene mutation preventing phosphorylation
  • serine mutation mimicked phosphorylation suggesting that phospho role is to destroy GRIP binding site
  • blocking LTD had no behavioral effects on eyeblink conditioning :(
22
Q

Bifurcated sensory neuron-two motor neuron synaptic tagging experiment

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A
  • apply 5x5HT to synapse M1 -> long-term (72h) EPSP to M1
  • apply 1x5HT to opposite synapse (M2) -> long-term EPSP to M2 as well now
  • apply phospho-CREB to nucleus of sensory neuron + 1x5HT in M1 synapse -> M1 synapse EPSP while M2 synapse intact

Evidence for:
- synaptic tag and its role in capturing the PRP mRNAs
- only 1x5HT needed to tag synapse
- transcription and CREB linked to 5x5HT

23
Q

Big idea of memory maintenance

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A

persistent kinases:
- generally, kinases are thought to drive memory in all sorts of way
- making them persitently active should increase memory maintenance

24
Q

Testing necessity of transcription for memory allocation

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A

Mark neurons that activated transcription during learning

Kill those neurons to see behavioral effects
- using CRE recombinase
- only neurons that transcribed after following CRE promoter activation from CREB will express toxin receptors and be killed by toxin

25
Why choose the lateral amygdala (LA) to study memory formation/allocation?
- closest model in vertebrates to the aplysia model - auditory-LA synapse acts as the sensory-motor neuron in aplysia
26
What does the CREB-DT condition represent in the LA memory allocation study?
- control condition - everything is same as experimental condition but there is no DT (toxin) receptors expressed in transcription neurons (or any neurons) - transcription neurons aren't killed but toxin is still injected
27
What does the CREB-cre, PBS condition represent in the LA memory allocation study?
- control condition - everything is same as experimental except they don't inject toxin - transcription neurons aren't killed bc no toxin
28
Testing sufficiency of transcription for memory allocation
- mark neurons activating transcription during learning of unharmful stimuli - optogenetic stimulations to those neurons to associate unharmful stimuli with shock
29
LTP in hippocampal model experiment
- 2 axons synapsing on 1 post-synaptic neuron - can induce LTP in synapse specific manner (S1 but not S2) 5x5HT in S1 -> protein synthesis inhibitor + 1x5HT in S2 - led to LTP at both synapses indicating that protein synthesis happens in a synapse non-specific manner - suggests tag formation is possible in presence of protein synthesis inhibitor - LTP induced in S2 until up to 1 hour after 5x5HT suggesting that the PRPs or the tag no longer works after an hour
30
Expression of dnKCNQ2 mimicked _______ ___________ during learning
CREB expression
31
What is excitability of a specific neuron thought to determine?
- thought to determine whether that neuron will activate transcription and therefore be part of a memory
32
Low levels of Arc non-dnKCNQ2 neurons compared to nearby dnKCNQ2-expressing neurons provide evidence that
- more excitable neurons are more likely to activate transcription and therefore be allocated to the memory - higher level of CREB allocates memory by increasing excitability
33
Low levels of Arc in Kir2.1-expressing neurons provides evidence that
- excitability of a neuron determines if it will activate transcription and be allocated to the memory
34
role of ubiquitin in memory maintenance
- ubiquitin destroys regulatory subunits of kinases after their dissociation - making persistent kinases -> maintenance
35
What happens to 5x5HT-related EPSP during injection of Rp-cAMPs?
- Rp-cAMPs is inhibitor of PKA - EPSP is blocked only up to 12h after 5HT treatment - suggests persistent PKA is maintaining memory until 12h after treatment - major implication: other process takes over memory maintenance after 12 hours
36
Mechanism to activate CAMKII
- Ca2+-calmodulin, together they bind to activate CAMKII - can be made persistently active with phosphorylation of next adjacent subunit only when Ca2+-Calmodulin is bound to subunit - so without Ca2+-Calmodulin, will not stay persistently active for too long -> cannot be responsible for long-term maintenance of memory
37
effects of CAMKII on memory formation and maintenance
- turns out CAMKII is important for memory induction but not due to its phosphorylating capacities: turning off them off didn't change memory induction - seems to have no role in memory maintenance
38
two mechanisms for persistent PKCs (PKMs)
- calpains removes regulatory subunit (sort of like PKA) - Transcript that encodes for already persistent PKC, PKC without regulatory subunit
39
ZIP is a ___ _____________ . What are its effects?
PKM inhibitor - it reverses maintenance and LT retention of spatial information
40
Injecting ZIP before recall of a 30 day old memory
- completely erased memory - suggests after one month, memory was still being maintained by something ZIP inhibited (presumably PKM) - blocking 90% of other protein kinases doesn't erase memory or stop maintenance
41
How does PKM act on synaptic strength?
- thought to block removal of AMPARs - blocking endocytosis with GluR23Y cancelled effect of ZIP --> evidence for above mentioned hypothesis
42
Reasons for skepticism about PKM zeta as memory maintenance protein
- knock out PKM zeta gene: memory is fine - ZIP is not super specific to PKM zeta, could be inhibiting another protein that is THE maintenance protein - ZIP still erases memory in mice with no PKM zeta - maintenance of memory normal in mice with no PKM zeta
43
PKC iota inhibitor in PKM zeta knock-out experiment
- ICAP (PKC iota inhibitor) erases memory in mice that do not express PKM zeta - suggests PKM zeta might really be involved in maintenance but PKC iota takes over when PKM zeta is gone
44
PKMs and LTF in aplysia
- Two sensory synapsing onto one MN - Induced LTF at one synapse and tag the other →LTF in both - Block PKMs w dn isoform →EPSP back to baseline in initial synapse but not in tagged synapse - Control substance blocked maintenance tagged synapse but not initial synapse - Suggests dif mechanisms
45
What did giving anisomycin after reminder of sensitization memory in aplysia do?
- erased memory at behavioral level - brought EPSP back to baseline (synaptic level) - aniso. without reminder did nothing - evidence for re-consolidation, memory is put in labile state when it is recalled
46
Evidence for savings
- LTF in aplysia - reminder + aniso (kills memory) - 3x5HT (typically not enough to drive LTF) - drives LTF - suggests there is savings from very first training session - same results with PKM inhibition
47
Potential cause of savings
- DNA methylation Method: - LTF in aplysia - protein synthesis inhibitor (kills memory) - 3x5HT (typically not enough to drive LTF) - drives LTF from savings Doing same procedure with DNA methylation inhibitor blocks sensitization and savings

PSYC 318 (3 decks)

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