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BS450 > Chapter 25: Molecular Mechanisms of Memory > Flashcards

Chapter 25: Molecular Mechanisms of Memory Flashcards

1
Q

iIdentifying where and how different types of
information are stored

A

neurobiology of memory

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2
Q

Accdg. to (), Memory results from synaptic modifications

A

Hebb

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3
Q

Study of simple invertebrates (Kandel)

molecular mechanisms lead to ()

A

synaptic plasticity

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4
Q

process by which some experiences, held temporarily by transient modifications of neurons, are selected for permanent storage in long-term memory

not all memories are created equal

A

memory consolidation

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5
Q

virtually () in the nervous system can form am memory of recent patterns of activity

A

all neurons

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6
Q

macaque monkeys can be trained to discriminate images of objects and associate them with a food reward; however, they can lose this ability when lesions are made in the ()

A

inferotemporal cortex (contains Area IT)

Area IT = both a visual area and an area involved in memory storage

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7
Q

selective amnesia for familiar faces (including one’s own) that can result from damage to the inferotemporal cortex in humans

A

prospagnosia

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8
Q

like most cortical neurons, IT neurons typically show the property of ()

A

stimulus selectivity

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9
Q

concept that a memory is represented by a unique pattern or ratio of activity of neuronal activity; no single neuron represents specific memory

A

distributed memory

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10
Q

memory loss: instead of a catastriohic loss of any one memory as a result of damaged neurons, representations tend to blend together as nwueons are lost -> one memory gets confused with another

A

graceful degradation of memories

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11
Q

synapses store memories

the () that leads to memory can be the modification of synaptic weight

A

physical change

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12
Q

Eric Kandel’s study of Aplysia californica showed that simple forms of learning (habituation, sensitization) were accompanied by changes in ()

A

strength of synaptic transmission between sensory neurons and motor neurons

they were able to dissect many of the molecualr mechanisms that underlie these changes

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13
Q

2 traditional views in memory research

A
  1. chain of reactions (Pavlov and Thorndike)
  2. flashbulb memory (insight learning)
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14
Q

memories formed as APs pass through pathways multiple times -> gradually, pathways are strengthened

A

chain of reactions

Conditioning

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15
Q

“one try learning”; being able to commit something to memory after experiencing it just once

evidence that chains of reactions cannot explain everything about memory formation

A

flashbulb memory (insight learning)

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16
Q

responses to a situation which are followed by a rewarding state of affairs will be strengthened and become habitual
responses to that situation.

A

Law of Effect (Thorndike)

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17
Q

() was thought to explain Flashbulb memory

A

Hebbian synapses

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18
Q

Connections between neurons increase in efficacy in proportion to the degree of correlation between pre- and post-synaptic activity.

“Neurons that fire together, wire together”

“Neurons that aren’t in sync, lose their link”

A

Hebb’s Rule

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19
Q

Hebbian explanation for short term memory: neruons activate each other

A

reverberation

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20
Q

Hebbian explanation for transition into long-term memory: when there are (1) that happen between active neurons, a new (2) is formed

A
  1. metabolic process
  2. functional assembly -> changes in synaptic weight
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21
Q

pattern completion based on Hebbian response

patterns are completed because synapses are ()

A

strengthened

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22
Q

even though part of the image is given, we can recollect the missing parts from memory

A

pattern completion

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23
Q
  1. () studies have shown that associative memories can be stored in a network of neurons using Hebbian learning rule (Hopfield, 1984).
  2. () is important.
  3. () serve this function in the brain.
A
  1. Neural network
  2. Bidirectional connectivity
  3. Recurrent collaterals
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24
Q

recurrent collaterals are especially present in the () -> epilepsy due to overactivity in this region is very common

A

hippocampus

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25
Q

well-known example of short-term synaptic plasticity in the NMJ

A

post-tectanic potentiation (PTP)

26
Q

increased response in PTP is due to ()

A

accumulation of Ca2+

27
Q

brief stimulation resulting in long-lasting response can explain ()

A

one time learning

28
Q

the hippocampus consists of 2 thin sheets of neurons folded onto each other

A
  1. dentate gyrus
  2. Ammon’s horn (cornu Ammonis, CA)
29
Q

the entorhinal cortex (major input to HC) sends info to the dentate gyrus of the HC via a bundle of axons called ()

A

perforant path

30
Q

dentate gyrus neurons give rise to axons called () that synapse on cells in CA3 (division of Ammon’s horn)

A

mossy fibers

31
Q

one of the branches that stem from CA3 neurons is called () -> synapse on CA1 neurons

other branch leaves HC via the fornix

A

Schaffer collateral

where the most sophisticated understanding of LTP was found

32
Q

LTP requires Ca2+ entry via (1); to open these, strong depolarization required to overcome (2)

A
  1. NMDA receptors
  2. Mg2+ block

NMDA receptor: coincidence detector (molecular switch)

33
Q

property in which only the activ inputs show synpatic plasticity

A

input specificity

34
Q

LTP induction is blocked by (1) and (2)

A
  1. AP5 (NMDA receptor blocker)
  2. EGTA (Ca2+ chelating agent)
35
Q

mechanism of LTP in CA1: increased [Ca2+] activates PKC and CaMKII, which in turn cause (3)

A
  1. phosphorylation of AMPA-Rs -> increased membrane conductance
  2. Increased number of AMPA-Rs at terminal
  3. Formation of new synapses (via formation of postsynaptic dendritic spines)
36
Q

(): synapses will undergo synaptic weakening instead of LTP when they are active at the same time the postsynaptic cell is only weakly depolarized by other input (1982).

A

BCM theory

37
Q

Bidirectional plasticity of many cortical synapses governed by two simple rules

A

– Synaptic transmission during strong depolarization of postsynaptic neuron causes LTP.
– Synaptic transmission during weak depolarization of postsynaptic neuron causes LTD.

38
Q

LTP can result when the EPSP caused by synaptic glutamate (excitatory) release precedes an AP in the postsynaptic neuron

A

spike timing-dependent plasticity

39
Q

Mechanisms of LTD in CA1

Two forms of controllimg homosynaptic LTD at Schaffer collateral–CA1 synapse

A

– G-protein coupled metabotropic glutamate receptors (mGluRs)
– NMDA receptors

40
Q

Rise in () is necessary to trigger LTD.

A

postsynaptic [Ca2+]

40
Q

() accounts for bidirectional
synaptic changes (up or
down)

A

partial block on NMDA-Rs (modest, prolonged elevation of Ca2+)

41
Q

() in the postsynaptic membrane are continually being added and removed (about every ~15 min)

A

AMPA receptors

42
Q

determine capacity of postsynaptic membrane for AMPA receptors

A

slot proteins (PSD-95)

43
Q

recent research suggests that the add’l receptors added to membrane during LTP contain ()

A

GluR1 subunits

44
Q

First evidence of NMDA receptor-dependent processes in memory

A

Morris experiments using water maze

45
Q

learning induces () in CA1

A

LTP

46
Q

Homeostatic mechanisms needed to provide stability and keep synaptic weights within useful dynamic range

A
  1. metaplasticity
  2. synaptic scaling
47
Q

Unchecked synaptic plasticity could lead to ()

A

unstable neuronal responses

further strengthening of synapses -> all synapses fully potentiated -> lose stimulus sensitivity0

48
Q
  • general idea that the rules of synaptic plasticity change depending on the history of synaptic or cellular activity
  • Adjustments in composition of NMDA receptors
A

metaplasticity

49
Q

metaplasticity

() increases in response to too much LTP (increased activity); same logic for too much LTD

A

synaptic modification threshold

50
Q

metaplasticity adjusts (), which determines the properties of NMDA receptors

A

NR2A/NR2B ratio (subunits in NMDA receptors)

more NR2B = favor LTP
more NR2A = favor LTD

51
Q
  • adjustment of absolute synaptic effectiveness that preserves the relative distribution of synpatic weights
  • Relative differences in synaptic strengths on a neuron are unchanged, even at the absolute levels go up or down
  • Occurs over hours to days
A

synaptic (homeostatic) scaling

52
Q

Other mechanisms needed for long-term consolidation

A
  • Persistently active protein kinases
    – Protein synthesis
53
Q

Persistently Active Protein Kinases:

(): large increase in [Ca2+] allows autophosphorylation -> maintains “on” state

A

CaMKII

54
Q

general idea that the an autophosphorylating inase could store information could store information at the synapse

A

molecular swtich hypothesis

in the context of CaMKII and LTP

55
Q

– “() zaps established memories”
– Maintains changes in synaptic strength by continuing to phosphorylate substrates

A

ZIP (PKM-zeta inhibitor)

56
Q

() required during the period of memory consolidation

A

New protein synthesis

when brain protein synthesis is inhibited, training of task is okay but no memory retention when tested days later

57
Q

Experiments of Julietta Frey and Richard Morris

  • Weak stimulation endows synapses with a ()
  • Enables them to capture newly synthesized proteins that consolidate LTP
A

tag

58
Q

with tag, an event that would otherwise be forgotten might be () if it occurs within 2 hours of a momentous event
that triggers a wave of new protein synthesis

A

seared into long-term memory

59
Q
  • Functions to regulate expression of neighboring genes (transcription factor)
  • regulates gene expression required for memory consolidation (fruit fly).
A

CREB: cyclic AMP response element binding protein

60
Q

– CREB-2 overexpression: (1)
– CREB-1 overexpression: (2)

A
  1. represses gene expression, blocks memory consolidation
  2. activates transcription, facilitates memory

BS450 (11 decks)

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