synaptic plasticity Flashcards
induction of LTD at CA3-CA1 synapse
NMDA receptor-dependent LTD
depenedent on activation of phosphatases
can be saturated and reversed
different LTD mechanism exist (mGluRs, VGCC, KARs)
expression of LTD at CA3-CA1 synapse
synaptic silecing may be a way of pruning syanpses during development
long-term depression
low frequency stimulation (LFS)
induces LTD at CA3-CA1 synapses
typical LFS used to induce LTD –900 stimuli delivered at 1 Hz (1 per second)
LTD is input specifi
frequency depenedent and NMDA LTP and LTD
deliver 900 pulses at a
range of frequencies
low frequencies = LTD
as frequency increases
magnitude of LTD
decreases
high frequencies = LTP
how can LTP and LTD both be dependent on NMDA receptor activation?
the size and time course of NMDA receptor activation and
calcium influx differ between LTP and LTD induction
LTP results from a large intracellular calcium rise for a short
period of time
LTD results from a smaller rise in calcium (over a longer time
scale)
enzymes (kinases/phosphatases) have different sensitivities to
calcium
kinases= excocytosis in AMPA
what is hebb’s postulate?
neurons that fire together, wire together
LTP and hebbian plasticity
synapses are strengthened when both the postsynaptic and presynaptic cell are active during the induciton protocol
NMDA receptor acts as a coincident detector – needs postsynaptic
depolarisation and presynaptic release of glutamate
LTD and anti-hebbian plasticity
synapses are weakened when both the presynaptic and postsynaptic cells are active during the induction protocol
bidirectional modifiable synapses
theta burst stimulation
decrease in trenamission from potentiation (de-potentiation)
useful for models of learning and memory
LTD in other brain regions
cerebellum- LTD occurs and is involved in motor learning
perihinial cortex- LTD occurs and is involved in object recognition (temporal lobe)
cerebellar LTD
stimulate parallel fibres coupled with depolarisation
of purkinje cell produces LTD
this is anti-hebbian
mechanisms of cerebellar LTD
requires activation
of both AMPA and
metabotropic
glutamate receptors
activation of protein
kinase C essential
AMPA receptors are
internalised, reducing number expressed at cell surface
does LTD=learning in perihinal cortex?
record from perirhinal cortex neurones; measure action potential firing;
Present picture of a novel object, neurones increase AP firing;
Present same image again, response of neurone is much reduced; LTD-like effect?
-induced by LFS
-input specific
-dependent on NMDA receptor activation
-LTD can be blocked by
putting a peptide into the postsynaptic cell that interferes with removal of AMPA receptors from the
cell surface
LTD in perihinal cortex of animals
using a virus to express same peptide in perirhinal cortex of animals blocks recognition memory
rats allowed to explore a novel and a familiar object. they will spend more time exploring the novel object. discrimination ratio is a measure of this – a ratio of 0 means the rat spends equal time
exploring the two objects
so peptide that blocks LTD in vitro also blocks learning in vivo