Shepard Flashcards

1
Q

what amount of time is remembered w/ short term memory

A

Lasts seconds to minutes (e.g. working memory of a telephone number).

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2
Q

what amount of time is remembered w/ long term memory

A

lasts days to years but constant “updating”

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3
Q

What does memory consilation depend on?

A

Consolidation of memory requires protein synthesis. Memories are
labile after retrieval and RE-consolidation is also protein synthesis-
dependent

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4
Q

how does different durations of memory effect synapses?

A
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5
Q

Habituation

A

non-associative procedural learning
decreasing response to a repeated stimulus
* Allows organisms to ignore unimportant stimuli
* e.g: Wearing clothes

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6
Q

Sensitization:

A

non-associative procedural learning
increasing response to all stimuli after an intense stimulus
* e.g.: Loud noises make you more sensitive to everything else
* Allows organisms to respond quickly in possibly dangerous situations

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7
Q

Classical Conditioning:

A

Associating a “meaningless” stimulus with a meaningful one* e.g: Pavlov’s dogs

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8
Q

Instrumental Conditioning:

A

Associating an action with an outcome
* e.g.: Lever-pressing

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9
Q

Habituation in Aplysia

A
  • Habituation is a presynaptic process (in this instance)
    – Repeated action potentials result in less Ca2+ influx into
    the cell
    – Less Ca2+ means less vesicle binding
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10
Q

Conditioning in Aplysia

A
  • Serotonin from L29 causes increase in cAMP
    – Same as in sensitization
  • If combined with depolarization, causes Ca2+ influx
  • Ca2+ causes adenylyl cyclase to produce cAMP much faster
  • Results in more phosphorylated K+ channels
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11
Q

duration of short term plasticity?

A

duration less than tens of minutes

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12
Q

Increase in synaptic strength

A

– Facilitation
– Augmentation
– Potentiation

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13
Q

Decrease in synaptic strength

A

– Depression

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14
Q

short term plastsicity n x p

A

Change in mean number of released vesicles =
n x p
* Mechanisms of pre-synaptic plasticity
– Change in probability of release, p
* Increase in p causes facilitation and potentiation
* Decrease in p causes depression
* Synapses with initial high p tend to depress
* Synapses with initial low p tend to potentiate
– Change in number of release sites, n

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15
Q

Paired Pulse Ratio

A

Ratio of second to first EPSP (or EPSC)
– Ratio different than 1 indicates plasticity
– Considered exclusively pre-synaptic
– Depression or facilitation may be observed
– Depression suggests initial release probability was
high
– Facilitation suggests initial release probability was low

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16
Q

Stages of LTP

A
  • Induction:
    – NMDA receptor dependent (usually) but sometimes
    voltage gated calcium channels
  • Expression:
    – Pre (change in vesicle release) or Post (AMPAR
    trafficking)
  • Maintenance:
    – Least known, requires protein synthesis and probably
    structural/actin changes
17
Q

Cellular mechanisms of LTP induction

A

– Cooperativity: multiple fibers
required for sufficient depolarization
of post-synaptic neuron
– Frequency dependence: high
frequency required for
depolarization to accumulate
– Associativity: high frequency of
strong pathway produces
depolarization for weak pathway

18
Q

Molecular mechanisms of LTP

A
  • NMDA receptor acts as a coincidence detector:
    – Blocking NMDA receptor prevents LTP
    – NMDAR activation requires post-synaptic
    depolarization and pre-synaptic glutamate release
    – Mg++blocks the NMDA receptor channel
    unless relieved by depolarization
  • Either summation of EPSPs or current injection
19
Q

NMDA receptors are….

A

coincidence detectors! (glutamate/depolarization)

also calcium permeable (Ca requisite for LTP)

20
Q

Calcium and Plasticity

A
  • Type of plasticity, i.e. depression versus potentiation
    depends on NMDA receptor activation, which
    controls calcium influx
    – Low activity =
    small calcium
    elevation = LTD
    – High activity =
    large calcium
    elevation = LTP
21
Q

Role of Ca2+/calmodulin-dependent protein
kinase II (CaMKII) in LTP

A
  • CaMKII activity is persistently activated after
    LTP induction
  • Inhibition of CaMKII
    activity blocks LTP
    and memory
    CaMKII phosphorylates AMPA receptors
  • Phosphorylation causes higher conductance and insertion
    of AMPA receptors
  • Increase in synaptic current in response to uncaged
    glutamate after LTP induction
22
Q

LTP expression mechanisms: AMPAR Trafficking

23
Q

ampa trafficking 2

25
26
Stages of LTD
Stages of LTD * Induction: * NMDA receptor dependent (usually) but other forms of LTD are induced by group 1 mGluRs. Homosynaptic vs heterosynaptic? Depotentiation? * Expression: * Pre (change in vesicle release) or Post (AMPAR trafficking) * Maintenance: * Least known, (sometimes) requires protein synthesis and probably structural/actin changes
27
Defects in activity-dependent gene transcription/translation result in...
cognitive disorders/autism
28
AMPA Trafficking LTD
29
Arc Protein is locally and rapidly translated in dendrites via
group 1 mGluRs
30
____ is required for mGluR/protein synthesis-dependent hippocampal LTD in CA1
Arc
31
Spike Timing Dependent Plasticity
* Pre-synaptic AP before post → LTP * Pre-synaptic AP may have contributed to post-synaptic activity * Pre-synaptic AP after post → LTD * pre-synaptic AP could NOT have contributed
32
Two ways to prevent runaway plasticity:
metaplasticity homeostatic plasticity
33
metaplasticity
(“state dependent plasticity”) Prior neuronal history of a cell/circuit changes the plasticity rules (not inherently homeostatic but can be)
34
homeostatic plasticity
Homeostatic Plasticity Processes that keep neuronal output constant, at a given set point AMPARs may scale
35
are memories stored in engrams?
Engram loss-of-function studies disrupt subsequent memory retrieval