In article <7ui3q4$fmm$1 at nnrp1.deja.com> Lawrence Ryan, loryan at sfu.ca
writes:
>And what is the trigger?
>With excitatory synapses, it's a level of correlation between excitatory
>input and backprop (among other things, perhaps). What triggers
>inhibitory LTP? Simply a frequency of inhibitory input above a threshold
>level?
There are a few different versions of inhibitory plasticity that have
been described. None of these is exactly like LTP familiar from
excitatory synapses. The time courses are generally shorter, etc. In the
case of one well studied version of inhibitory LTP/LTD between Purkinje
cneurons and deep cerebellar nucleus neurons (see papers by Aizenman and
Linden), the mechanism is something like this: An IPSP results in a
hyperpolarization which removes calcium and sodium channels from their
inactivated state, and during the decay phase of the IPSP (that is,
during the depolarizing ramp) these channels help to launch a "rebound
spike", with accompanying calcium influx. A train of IPSPs gives a larger
number of rebound spikes (because it removes more voltage-gated channels
from inactivation), with a larger calcium influx. The amount and polarity
of LTP or LTD that results is a function of the amount of spiking (and
presumably calcium). The connection between the calcium influx and the
modification of synaptic strength is as mysterious at this synapse as it
is for excitatory synapses.
Cheers,
Matt Jones
