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Cell and Molecular Neuroscience > Shepard > Flashcards

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

A
23
Q

ampa trafficking 2

A
24
Q
A
25
Q
A
26
Q

Stages of LTD

A

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
Q

Defects in activity-dependent gene transcription/translation result in…

A

cognitive disorders/autism

28
Q

AMPA Trafficking LTD

A
29
Q

Arc Protein is locally and rapidly translated in dendrites via

A

group 1 mGluRs

30
Q

____ is required for mGluR/protein synthesis-dependent
hippocampal LTD in CA1

A

Arc

31
Q

Spike Timing Dependent Plasticity

A
  • 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
Q

Two ways to prevent runaway plasticity:

A

metaplasticity
homeostatic plasticity

33
Q

metaplasticity

A

(“state dependent plasticity”)
Prior neuronal history of a cell/circuit changes the plasticity rules (not
inherently homeostatic but can be)

34
Q

homeostatic plasticity

A

Homeostatic Plasticity
Processes that keep neuronal output constant, at a given set point
AMPARs may scale

35
Q

are memories stored in engrams?

A

Engram loss-of-function studies disrupt
subsequent memory retrieval

Cell and Molecular Neuroscience (15 decks)

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