lecture 10 part 2 Flashcards
(16 cards)
hebbian
correlated pre and post synaptic activity produces long term enhacnement of connection
or neurons that fire together wire together
where is hebbian plasticity found
rodent hippocampus from CA3-CA1
long term potentiation of Schaffer collateral CA1 synapse
a brief high frequency train of stimuli to Schaffer collaterals causes LTP as a long lasting increase in EPSP amplitude
specificity to pathway tetanus is induced in
is firing necesarry for hebbian plasticity
no but depolarization is
fire presynaptic afferants and depolarize post synaptic
specificity and associativity
specificity- strong activiaty intiiated LTP at active synapse without initiating LTP at nearby inactive synapse
associativity- strong stimulation activated with weak stimulation causes both synaspes to be strengthened
NMDA receptor mechanism in LTP
NMDA receptors can only flux Ca and cause LTP if depolarized (expel Mg)
molecular coincidance detector: need glutamate and depolarization
what happens to cells at resting potential
only AMPA can flux Na and no LTP can occur
what effect do Ca chelators have on LTP
fast chelators gather up Ca and block it from activating CAMKII and phosphorylating AMPA receptors to be inserted therefor blocking LTP
prevent back propogating APs from raising Ca
LTP and AMPA
LTP causes an increase in glutamate response of a dendritic spine due to an increase in # of AMPA receptors on spine membrane
can be seen using color scale
silent vs functional synapses
silent - NMDA only
functional- AMPA and NMDA
protein synthesis in LTP
required for maintaining LTP
PKA activates CREB which turns on expression of genes that produce long lasting changes in synaspe
both plasticity in Aplysia synapse and LTP in hippocampus
bohth show the same features of early transient phase relying in protein kinases to produce post translational changes in existing proteins and
long lasting phases that require gene expression
both mediated by CREB, calmodulin, Ca, cAMP
LTP and LTD
both require NMDA
large fast NMDA: Ca increases trigger LTP
protein phosphrylation leads to AMPA insertion
small slow NMDA: Ca leads to LTD
Ca dependant phosphatases lose AMPA
spike timing dependant plasticity
precise timing of pre and post activity determines polarity of LTD or LTP
LTD in cerebellum
climbing fiber wraps around dendrite and makes many contacts so it can cause purkinje cell to fire many spikes is associative (unlike LTD) needs coincidence input
mechanism of LTD in cerebellum
high calcium in spine leads to removal of AMPA receptors
glutamate binds to AMPA and mGluR to internalize AMPA receptors
need: calcium induced calcium release at the same time as climbing fiber input depolarization
