STDP and LTP
jonesmat at physiology.wisc.edu
Fri Sep 20 11:29:38 EST 2002
herwin at theworld.com (Harry Erwin) wrote in message news:<1fi9hw2.1ejd5a81p4af44N%herwin at theworld.com>...
> I've been trying to resolve the differences between spike timing
> dependent plasticity and Bliss and Collingwood LTP. The former involves
> a single synapse and a BAP _after_ the EPSP, while the latter involves
> _prior_ depolarization when the NMDA receptor is stimulated. They seem
Spike timing dependent plasticity can be either potentiation or
depression. Potentiation if the postsynaptic cell fires repetitively
-after- the presynaptic spike, and depression if it fires before the
In this sense, it appears incompatible with traditional LTP where the
postsynaptic cell is depolarized before or during the presynaptic
However, the two protocols are very different. Traditional LTP uses
whopping huge depolarizations and and huge calcium influxes, whereas
single-spike plasticity is working over a range of intracellular
calcium that is much lower, and probably changing rapidly instead of
just flooding the postsynaptic cell continuously.
I'm not sure of the exact connection (and by the way, have the STDP
studies of Bi and Poo been repeated by any other labs?). However the
work of Mark Bear and others might help to understand the relation
between the two protocols better.
Their idea is that there is a "sliding scale" of calcium that
determines whether you get potentiation or depression. Low calcium
fluxes tend to cause depression, and higher ones tend to cause
potentiation. This is why traditional LTP protocols use humongous
tetanic bursts, and LTD protocols use very long 1Hz trains. The former
lets in a lot of calcium, whereas the latter elevates calcium only
In the context of STDP, then, a backpropagating spike that occurred
before the presynaptic spike might cause just a little elevation in
calcium, leading to depression, whereas repetitive spiking after the
presynaptic spike might cause more calcium entry, because the NMDA
receptors that were activated by the presynaptic spike would
transiently unblock during each postsynaptic spike, letting in a lot
I know that was pretty vague. Just a guess at a possible way of
reconciling the two types of plasticity.
I repeat that i am curious as to whether STDP has been demonstrated in
any other labs. If one does a medline search for "spike timing
plasticity", one turns up an awful lot of theoretical papers, but not
very many experimental ones.
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