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psyc 318 > memory maintenance > Flashcards

memory maintenance Flashcards

1
Q

how should memories be maintained

A

biochemical trace needs to be maintained

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2
Q

how can biochemical trace be maintained (4)

A
  1. persistent protein kinases retain phosphorylation of synaptic proteins
  2. insertion of membrane proteins (like AMPAR) maintained
  3. structural changes (size of synapse) may be long-lasting
  4. new synapses
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3
Q

what process may be required for memory erasure

A

AMPAR endocytosis

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4
Q

structure of protein kinases (like PKA) in inactive state

A
  1. 2 domains: regulatory & catalytic
  2. binding of pseudosubstrate keeps both domains linked together -> inactive
  3. pseudosubstrate stops kinase from phosphorylating things
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5
Q

which domain makes protein kinases inactive

A

regulatory domain

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6
Q

structure of protein kinases (like PKA) in active state (3)

A
  1. 2nd messenger binds to regulatory domain -> causes conformational change
  2. regulatory and catalytic domains no longer linked -> active
  3. catalytic domain can phosphorylate things
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7
Q

role of anchoring proteins that bind to protein kinases

A

bring the protein kinase to appropriate substrate

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8
Q

how does PKA become persistently active

A

regulatory domain ubiquitinated and targeted for proteolysis

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9
Q

structure of PKA, how becomes active and persistent activity

A
  1. separate regulatory and catalytic subunits
  2. cAMP binding causes dissociation of subunits
  3. timing to re-bind is important
  4. degradation of regulatory subunit leads to persistent activity of PKA and leaves molecular memory trace
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10
Q

how test for induction of memory trace

A

inhibiting process (kinase) before or during experience tests

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11
Q

how test for mechanisms involved in maintaining trace

A

inhibiting process (kinase) after experience

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12
Q

effect of inhibiting PKA (during stimulation with 5HT)

A
  1. removes increase in synaptic strength (LTF) for 12 hours after stimulation
  2. after 12h, no more effect of inhibitor
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13
Q

what did experiment inhibiting PKA lead to conclude

A

that mechanism for memory maintenance changes bw 12 and 24 h

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14
Q

what is camkii and how is it activated

A
  1. kinase activated by calcium influx
  2. dodecamer
  3. calcium binds to calmodulin and both bind kinase and activate it
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15
Q

how does camkii become constitutively active

A

phosphorylation by neighboring subunit (autophosphorylation) -> cascade of phosphorylation

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16
Q

limits to persistent activation of camkii (2)

A
  1. critical site cannot be rephosphorylated in absence of calmodulin (calcium-camodulin acting as substrate (bound) is required)
  2. after end of stimulation, phosphatases remove phosphates on subunits -> inactivation
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17
Q

technique to measure camkii activation in-situ + explain (4)

A
  1. FRET -> measure distance bw 2 fluorophores
  2. add fluorophore to kinase -> activation of kinase changes distance
  3. inactive camkii -> fluorophores close together so red emission (FRET transfer of energy)
  4. active camkii -> confo change, fluorophores far from eo so no energy transfer
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18
Q

results of measure camkii activation with fret (4)

A
  1. camkii is transiently activated
  2. becomes inactie after 1 min
  3. however, spine got bigger (sign of LTP)
  4. camkii important for induction of memory, but not for maintenance of memory
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19
Q

what is camkii important for

A

induction of memory

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20
Q

other than autophosphorylation, what other way can camkii be persistently activated

A

directly binding to NMDARs that lock it into an active state

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21
Q

effect of losing interaction bw camkii and NMDARs (3)

A
  1. only minor learning impairments
  2. LTP induction inhibited
  3. maintenance not affected
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22
Q

adding camkii inhibitor (a) before inducing ltp, (b) after inducing ltp

A

before: blocks ltp (memory induction)
after: does nothing (memory still maintained)

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23
Q

what causes persistent activation of pkc

A

loss of regulator domain (similar to pka)

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24
Q

difference bw pkc and pka structure (2)

A

pkc: regulatory and catalytic domain on same molecule (~ camkii) + no phosphorylation site that leads to persistent activation

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25
Q

mechanisms of creating persistently activated pkc (2)

A
  1. translating transcript that lacks regulatory domain
  2. proteolysis that separates regulatory and catalytic domains
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26
Q

what disrupts pkc maintenance of ltp

A

inhibitors of pkm zeta (ZIP)

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27
Q

name of pkc without regulatory domain

A

pkm zeta

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28
Q

administration of zip (a) 24h after induction of ltp, (b) 1h after induction of ltp

A

(a) decrease of synaptic strength (loss of memory maintenance)
(b) no effect

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29
Q

what is pkm (zeta) important for

A

late maintenance of memory (not early maintenance of memory)

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30
Q

what molecule reverses ltp (24h)

A

zip (pkm zeta inhibitor)

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31
Q

pkm zeta inhibition and retention of spatial information (experiment of mouse on rotating arena)

A
  1. mouse learns where it is by looking + gets shock in 1 area
  2. after training avoids area where shock delivered
  3. after 24h + saline -> retains information: avoids area where shock delivered
  4. after 24h + zip -> no recall: goes everywhere even where received shock
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32
Q

is administration of zip like ablating area in hippocampus and why

A

no; can retrain animal so it recalls

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33
Q

what type of memory does zip block

A

blocks ltm, not stm

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34
Q

effect of injecting staurosporine 24h after inducing ltp on memory storage

A

doesn’t block memory maintenance

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35
Q

effect of injecting zip 30 days after induction of ltp

A

erases memory

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36
Q

ex of memory sensitive to zip and ex of memory not sensitive to zip

A

sensitive -> taste aversion (up to 3 months)
insensitive -> identification of novel taste

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37
Q

effect of zip on (a) auditory/contextual fear conditioning, (b) remembering pain, (c) drug-induced place preference

A

(a) both blocked by zip in LA
(b) inhibits recall of pain
(c) inhibits recall of preferred place

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38
Q

effect of overexpressing pkm zeta on receptors

A

increase in ampar number

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39
Q

possible mechanism of pkm zeta

A

blocking endocytosis of ampars

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40
Q

inhibition oh pkm zeta on ampars

A

ampars removed from pm and memory is lost

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41
Q

what rescues effects of zip

A

blocking endocytosis of ampars

42
Q

what is glur23y and what does it do + effect on zip

A

peptide from glua2 that blocks endocytosis of glua2 by competing with endocytic adaptors -> rescues effect of zip (don’t lose memory maintenance)

43
Q

effect of pkm zeta ko on (a) learning, (b) action of zip on ltp, (c) maintenance of memory

A

(a) normal learning
(b) zip still erases ltp and memory
(c) normal ltp maintenance

44
Q

what are possibilities that explain that zip sill works in pkm zeta ko (2)

A
  1. target of zip is something else
  2. compensation by upregulating other memory molecule also blocked by zip
45
Q

effect of pkc iota inhibitor in (a) pkm zeta ko, (b) normal; and why

A

(a) blocks maintenance of memory -> pkm zeta absent so pkc iota upregulated (inhibitor has impact)
(b) no decrease in maintenance of memory -> pkm zeta present so no need to upregulate pkc iota (inhibitor has no effect)

46
Q

experiment of mouse on rotating arena -> injecting pkc iota inhibitor in (a) wt (b) pkm zeta ko

A

(a) learn where get shocked + retain info when injected with pkci inhibitor
(b) learn where get shocked + don’t remember when injected with pkci inhibitor (go where get shocked)

47
Q

what supports that there are distinct molecular complexes at synapses supporting memory

A

zip erases memory without affecting regular synaptic functions

48
Q

mechanisms of forgetting (2)

A
  1. passive loss of trace
  2. active removal of trace
49
Q

what is passive loss of trace

A

normally active phosphatases remove phosphorylation when kinase becomes inactive

50
Q

what is active removal of trace

A

circuit activates phosphates to remove trace

51
Q

what is rac important for + role in memory

A

regulating actin cytoskeleton (and other processes); role (+) in active forgetting

52
Q

effect of overexpression of dnRac

A

prolongs memory retention without affecting learning

53
Q

effect of overexpressing rac

A

shortens memory without affecting learning

54
Q

what is reversal learning

A

erasing 1st memory when later experiences show its wrong

55
Q

role of rac in reversal learning

A

important for reversal learning because dnRac prevents reversal learning

56
Q

effect of light on photoactivable rac-tagged spines + conclusion

A

light activates rac -> shrinking of spines + forgetting
conclusion -> part of learning is inhibiting active forgetting (rac is inhibited to remember)

57
Q

ways to reduce normal forgetting (2)

A
  1. inhibit rac
  2. prevent ampar endocytosis
58
Q

effect of inhibiting ampar endocytosis on STM

A

prolongs memory that would normally decay (STM)

59
Q

what protein might mimic he mechanism of active forgetting

A

pkm (inhibition)

60
Q

what process do inhibitors like zip mimic

A

active forgetting system (to erase memory)

61
Q

how are active forgetting and erasure related

A

they both require endocytotic event

62
Q

what processes does reconsolidation depend on

A

transcription and protein synthesis

63
Q

recall of a memory puts a memory in which state

A

labile state where it needs reconsolidation (when memory can be updated, changed) -> vulnerable

64
Q

what experimental manipulations can lead to loss of memory

A

giving a reminder trial (of shock) followed by inhibitor of protein synthesis -> no protein synthesis, no reconsolidation, memory loss

65
Q

inhibitor of protein synthesis (ex)

A

anisomycin (aniso)

66
Q

effect of injecting aniso (a) during reminder, (b) without reminder (24h later)

A

(a) lose memory (that animal recalled)
(b) don’t lose memory because have nothing to recall

67
Q

aplysia: during sensitization, strong correlation bw … and …

A

new synapses and (longer-lasting) memory

68
Q

if new synapses not formed (aplysia) how long does memory last

A

24h

69
Q

effect of memory formation (rodents) on spine formation

A

stabilization of new spines (increase in some spines, decrease in other spines (number invariant) -> new spines maintained if learning happens)

70
Q

effect of putting rodents in enriched environment on spine formation

A

large increase in number of synapses

71
Q

why are new synapses a parallel process for generating memory

A

formation of new synapses and stabilization takes hours and can’t contribute to stm formation

72
Q

use what to study relationship bw new synapses and erasure (2)

A
  1. sensitization behavior (withdrawal response)
  2. ltf in sensory-motor neuron cultures
73
Q

effect of injecting aniso after reminder on (a) response to shock (b) sensitization response (withdrawal) (c) ltf (d) varicosity number

A

(a) decreased freezing (forgets)
(b) decreased withdrawal (forgets)
(c) decreased ltf
(d) decreased amount of (non-specific) varicosities

74
Q

do varicosities = synapses?

A
  1. not all synapses are at varicosities
  2. not all varicosities contain synapses
75
Q

effect of pkm inhibition on sensitization, ltf and varicosity number

A

all decrease

76
Q

what are savings

A

even when memory not expressed, may be traces that remain -> revealed with spontaneous recovery or when relearning occurs faster than before

77
Q

what kind of changes do savings experiments implicate

A

nuclear changes that remain after memory erasure

78
Q

what does a suboptimal stimulus lead to

A

memory formation after reconsolidation

79
Q

what is a suboptimal stimulus

A

stimulus that doesn’t require transcription to be activated

80
Q

effect of reminder + aniso compared to reminder + aniso + suboptimal stimulus h later

A

reminder + aniso -> memory loss
with suboptimal stimulus -> initially forget (aniso), able to relearn because of suboptimal stimulus (recall same as control)

81
Q

effect of reminder + pkm inhibition compared to reminder + pkm inhibition + suboptimal stimulus h later

A

reminder + pkm inhibition -> memory loss
with suboptimal stimulus -> initially forget (pkm inhibition), able to relearn because of suboptimal stimulus (recall same as control)

82
Q

what is epigenetics

A

changes in which genes are expressed because of changes in histones (acetylation) and dna modifications (methylation)

83
Q

what are hats

A

histone acetylases -> acetylate histones around transcription start site, freeing up dna so rna polymerase can bind and translate (increased transcription of dna)

84
Q

what are hdacs

A

histone deacetylases -> remove acetyl groups from dna, tightening histones and making dna unavailable to rna (decreased transcription of dna)

85
Q

what does a hdac inhibitor do

A

leads to increased histone acetylation and increasing transcription

86
Q

effect of administration of pkm inhibitor and hdac inhibitor after ltp induction

A

normal sensitization response (like control) -> no memory loss

87
Q

administration of hdac inhibitor before ltp induction after 24h

A

activates learning -> creation of sensitization response (same as if trained with 5HT)

88
Q

hdac inhibitors are similar to which cellular process

A

removing creb repressor

89
Q

how do hdac inhibitors affect stimulus that normally only leads to stm

A

turns stimulus into one that leads to ltm

90
Q

how do hdac inhibitors turn stimulus that leads to stm to stimulus that leads to ltm

A

making transcription easier to activate (keeping chromatin more open)

91
Q

action of hdac inhibitors on pkm inhibitors and what does this mean for savings/memory

A

block actions of pkm inhibitors -> savings can reestablish memory if transcription is ongoing

92
Q

how does dna methylation change dna

A

adds methyl on cytosine of cpg sites

93
Q

when does methylation occur and how is it retained

A

occurs during cell fate determination; retained after cell division by enzymes that copy methyl group as dna is replicated

94
Q

role of dnmt (2)

A
  1. retain methylation on dna
  2. required for ltm (maybe turning off memory repressors)
95
Q

what do methyl-cpg-binding (mbd) proteins do (2)

A
  1. attract repressors and hdacs
  2. are the effectors of dna methylation
96
Q

effect of methylation on gene expression

A

target gene silenced (not transcribed)

97
Q

proposed pkm inhibition mechanism (DNA level)

A

pkm inhibition (erasure) removes acetylation on dna, but leaves methylation -> savings

98
Q

effect of inhibiting dna methylation before ltm induction (2)

A
  1. blocks memory formation
  2. blocks savings
99
Q

how can memory be erased (2)

A
  1. blocking pkm
  2. reconsolidation
100
Q

what could savings be due to

A

lower levels of repressors of memory formation

101
Q

aspects of memory stored in nucleus (2)

A
  1. histone modifications
  2. dna methylation
102
Q

what measures memory maintenance (2)

A
  1. forgetting
  2. erasure

psyc 318 (6 decks)

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