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- From: wcalvin@stein.u.washington.edu (William Calvin)
- Newsgroups: bionet.neuroscience
- Subject: Re: primary afferent depolarization
- Message-ID: <1k16ugINNrqb@shelley.u.washington.edu>
- Date: 25 Jan 93 17:10:40 GMT
- References: <9301251254.AA21883@xray1.cshl.org>
- Distribution: bionet
- Organization: University of Washington
- Lines: 30
- NNTP-Posting-Host: stein.u.washington.edu
-
- anderson@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@U.Washington.edu
- University of Washington NJ-15
- Seattle, Washington 98195 FAX:1-206-720-1989
-