anderson at CSHL.ORG (John Anderson) writes:
>I have been reading
> Sykova E. (1991) "Activity-related ionic and volume changes in
> neuronal microenvironment" in _Volume Transmission in the Brain_ (K.
> Fuxe, L.F. Agnati, Eds.), pp 317-336, Raven Press, New York.
>In that article, the following statement is made:
> "[Extracellular] K+ accumulation has been accepted as one of two
> causal factors (together with GABA) in primary afferent
> depolarization, which is the mechanism underlying presynaptic
> inhibition. It is assumed that the increase in [K+]e that is
> associated with repetitive neuronal activity reduces transmitter
> release by curtailing the presynaptic spike amplitude by presynaptic
> depolarization."
>Could someone please explain this statement? How does presynaptic
>depolarization reduce the presynaptic spike amplitude? Seems like it
>should enhance it.
Repetitive activation of neurons dumps some K outside the cell; like a
local hormone, it *may* reduce membrane potentials of other neurons. What
this does to transmitter release by spikes depends on accomodation-like
factors such as sodium inactivation and such. The invading spike may stop
*actively* propagating upstream and only passively invade the terminal, so
that the spike height stimulating transmitter release is smaller.
There are other factors as well, both on that hypothesis and on other
causes of presynaptic inhibition.
William H. Calvin WCalvin at U.Washington.edu
University of Washington NJ-15
Seattle, Washington 98195 FAX:1-206-720-1989
