synaptic plasticity

who came up with 1894 theory memories might be formed by strengthening of connections between neurons

santiago ramon y caial

whos theory was in 1949

donald hebb

what was hebbian theory

When an axon of cell A is near enough to excite cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells such that A’s efficiency, as one of the cells firing B, is increased

basis of hebbian theory

weak connection between A and B

when A and B fire action potentials at the same time the connection between them becomes stronger

neurons that fire together…

wire together

connections made by

synapses

concept of synaptic plasticity

the strength of synaptic communication between 2 neurons is not fixed

what is synaptic plasticity the change in

strength of synaptic communication

CA1 fEPSPs (extrinsic post synaptic potential) exhibit what

short term plasticity

two stimuli in quick succession whats diff between 1st and 2nd

2nd is larger than st

synapses can also exhibit long term changes in what

synaptic strength

who came up with the first description of long term potentiation of synaptic strength

Bliss and Lomo

what did bliss and lomo do

recordings of fEPSPs in the perforant pathway of anaethetised rabbits

measuring changes to synaptic strength

long term potententiation

high frequency conditioning stimulus what happened to amplitude

increased and stayed high

4 key properties of LTP

input specificity, associativity, cooperativity, persistence

what is input specificity

change in synaptic strength occurs only at those synapses that are activated between a presynaptic and postsynaptic neuron that are simultaneously active

what is associativity

where there's a weak stimulus in one particular pathway may not be sufficient to elicit LTP activation its own

When paired with activity in another strong pathway = LTP in both pathways

whats cooperativity

similar to associativity but  does not require the second pathway to have a strong stimulus à just several input pathways activated at the same time

LTP is persistent what does this mean

when theres an increase in synaptic strength it can last across the time

what does APV act as

selective NMDA receptor agonist

whats required for LTP

NMDA receptors

where are NMDA receptors activated

depolarised potentials

when is Mg block removed

depolarisation

why are NMDA receptors called coincidence receptors

can detect pre and post synaptic activity

what can NMDA receptors do at the same time

detct. presynaptic activity of glutamate and postsynaptic activity (depolarisation)

glutamate opens what

NMDA receptor

Magnesium blocks what in presence of glutamate

NMDA receptor

what activates the intracellular signalling cascade

influx of Ca2+ ions

in the off state on CaMKII where are the active sites

clustered around the pore

what turns CaMKII on

Ca2+ binding

What happens to turn CaMKII on

conformational change - release of active sites so that they can ho and phosphorylate downstream effectors activating them

list some presynaptic ways that LTP is expressed

change is release properties: increase number of release sites, increase cleft glu concentration

mechanisms postsynaptic by which LTP is expressed

change in AMPA properties, change in AMPAR number

what determines whether the expression of LTP is pre or post

the synapse

where is LTD found

found at many synapses in the brain, hippocampus

how is LTD achieved

by prolonged low frequency stimulation

what are some forms of LTD dependent on

NMDA receptor activation

NMDA receptor what blcok LTD

agonist D-APV

some forms of LTD are dependent on what

NMDA receptor activation and postsynaptic Ca2+ entry

what does intracellular Ca2+ chelation use to block LTD

BAPTA

name 2 other mechanisms LTD can be induced

activation of metabotropic glutamate receptors

activation of muscarinic acteylcholine receptors

process of how neuronal networks remember things

encoding - consolidation - recall

high frequency stimulation

NMDA receptor activation

• ca2+ influx activates intracellular cascades

low frequency stimulation

• NMDA receptor activation

• mGluR activation

• mAChR activation

different patterns of synaptic (and NMDA receptor) activation leads to different outcomes?

LTP or LTD