Shepard Flashcards
what amount of time is remembered w/ short term memory
Lasts seconds to minutes (e.g. working memory of a telephone number).
what amount of time is remembered w/ long term memory
lasts days to years but constant “updating”
What does memory consilation depend on?
Consolidation of memory requires protein synthesis. Memories are
labile after retrieval and RE-consolidation is also protein synthesis-
dependent
how does different durations of memory effect synapses?
Habituation
non-associative procedural learning
decreasing response to a repeated stimulus
* Allows organisms to ignore unimportant stimuli
* e.g: Wearing clothes
Sensitization:
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
Classical Conditioning:
Associating a “meaningless” stimulus with a meaningful one* e.g: Pavlov’s dogs
Instrumental Conditioning:
Associating an action with an outcome
* e.g.: Lever-pressing
Habituation in Aplysia
- 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
Conditioning in Aplysia
- 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
duration of short term plasticity?
duration less than tens of minutes
Increase in synaptic strength
– Facilitation
– Augmentation
– Potentiation
Decrease in synaptic strength
– Depression
short term plastsicity n x p
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
Paired Pulse Ratio
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
Stages of LTP
- 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
Cellular mechanisms of LTP induction
– 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
Molecular mechanisms of LTP
- 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
NMDA receptors are….
coincidence detectors! (glutamate/depolarization)
also calcium permeable (Ca requisite for LTP)
Calcium and Plasticity
- 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
Role of Ca2+/calmodulin-dependent protein
kinase II (CaMKII) in LTP
- 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
LTP expression mechanisms: AMPAR Trafficking
ampa trafficking 2
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
Defects in activity-dependent gene transcription/translation result in…
cognitive disorders/autism
AMPA Trafficking LTD
Arc Protein is locally and rapidly translated in dendrites via
group 1 mGluRs
____ is required for mGluR/protein synthesis-dependent
hippocampal LTD in CA1
Arc
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
Two ways to prevent runaway plasticity:
metaplasticity
homeostatic plasticity
metaplasticity
(“state dependent plasticity”)
Prior neuronal history of a cell/circuit changes the plasticity rules (not
inherently homeostatic but can be)
homeostatic plasticity
Homeostatic Plasticity
Processes that keep neuronal output constant, at a given set point
AMPARs may scale
are memories stored in engrams?
Engram loss-of-function studies disrupt
subsequent memory retrieval
