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
well-known example of short-term synaptic plasticity in the NMJ
post-tectanic potentiation (PTP)
26
increased response in PTP is due to ()
accumulation of Ca2+
27
brief stimulation resulting in long-lasting response can explain ()
one time learning
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the hippocampus consists of 2 thin sheets of neurons folded onto each other
1. dentate gyrus 2. Ammon's horn (cornu Ammonis, CA)
29
the entorhinal cortex (major input to HC) sends info to the dentate gyrus of the HC via a bundle of axons called ()
perforant path
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dentate gyrus neurons give rise to axons called () that synapse on cells in CA3 (division of Ammon's horn)
mossy fibers
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one of the branches that stem from CA3 neurons is called () -> synapse on CA1 neurons ## Footnote other branch leaves HC via the fornix
Schaffer collateral ## Footnote where the most sophisticated understanding of LTP was found
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LTP requires Ca2+ entry via (1); to open these, strong depolarization required to overcome (2)
1. NMDA receptors 2. Mg2+ block ## Footnote NMDA receptor: coincidence detector (molecular switch)
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property in which only the activ inputs show synpatic plasticity
input specificity
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LTP induction is blocked by (1) and (2)
1. AP5 (NMDA receptor blocker) 2. EGTA (Ca2+ chelating agent)
35
mechanism of LTP in CA1: increased [Ca2+] activates PKC and CaMKII, which in turn cause (3)
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
(): 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).
BCM theory
37
Bidirectional plasticity of many cortical synapses governed by two simple rules
– Synaptic transmission during strong depolarization of postsynaptic neuron causes LTP. – Synaptic transmission during weak depolarization of postsynaptic neuron causes LTD.
38
LTP can result when the EPSP caused by synaptic glutamate (excitatory) release precedes an AP in the postsynaptic neuron
spike timing-dependent plasticity
39
# Mechanisms of LTD in CA1 Two forms of controllimg homosynaptic LTD at Schaffer collateral–CA1 synapse
– G-protein coupled metabotropic glutamate receptors (mGluRs) – NMDA receptors
40
Rise in () is necessary to trigger LTD.
postsynaptic [Ca2+]
40
() accounts for bidirectional synaptic changes (up or down)
partial block on NMDA-Rs (modest, prolonged elevation of Ca2+)
41
() in the postsynaptic membrane are continually being added and removed (about every ~15 min)
AMPA receptors
42
determine capacity of postsynaptic membrane for AMPA receptors
slot proteins (PSD-95)
43
recent research suggests that the add'l receptors added to membrane during LTP contain ()
GluR1 subunits
44
First evidence of NMDA receptor-dependent processes in memory
Morris experiments using water maze
45
learning induces () in CA1
LTP
46
Homeostatic mechanisms needed to provide stability and keep synaptic weights within useful dynamic range
1. metaplasticity 2. synaptic scaling
47
Unchecked synaptic plasticity could lead to ()
unstable neuronal responses ## Footnote further strengthening of synapses -> all synapses fully potentiated -> lose stimulus sensitivity0
48
- general idea that the rules of synaptic plasticity change depending on the history of synaptic or cellular activity - Adjustments in composition of NMDA receptors
metaplasticity
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# metaplasticity () increases in response to too much LTP (increased activity); same logic for too much LTD
synaptic modification threshold
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metaplasticity adjusts (), which determines the properties of NMDA receptors
NR2A/NR2B ratio (subunits in NMDA receptors) ## Footnote more NR2B = favor LTP more NR2A = favor LTD
51
* 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
synaptic (homeostatic) scaling
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Other mechanisms needed for long-term consolidation
- Persistently active protein kinases – Protein synthesis
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# Persistently Active Protein Kinases: (): large increase in [Ca2+] allows autophosphorylation -> maintains "on" state
CaMKII
54
general idea that the an autophosphorylating inase could store information could store information at the synapse
molecular swtich hypothesis ## Footnote in the context of CaMKII and LTP
55
– “() zaps established memories” – Maintains changes in synaptic strength by continuing to phosphorylate substrates
ZIP (PKM-zeta inhibitor)
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() required during the period of memory consolidation
New protein synthesis ## Footnote when brain protein synthesis is inhibited, training of task is okay but no memory retention when tested days later
57
# Experiments of Julietta Frey and Richard Morris - Weak stimulation endows synapses with a () - Enables them to capture newly synthesized proteins that consolidate LTP
tag
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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
seared into long-term memory
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- Functions to regulate expression of neighboring genes (transcription factor) - regulates gene expression required for memory consolidation (fruit fly).
CREB: cyclic AMP response element binding protein
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– CREB-2 overexpression: (1) – CREB-1 overexpression: (2)
1. represses gene expression, blocks memory consolidation 2. activates transcription, facilitates memory