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- Path: sparky!uunet!wupost!uwm.edu!biosci!CSHL.ORG!anderson
- From: anderson@CSHL.ORG (John Anderson)
- Newsgroups: bionet.neuroscience
- Subject: primary afferent depolarization
- Message-ID: <9301251254.AA21883@xray1.cshl.org>
- Date: 25 Jan 93 12:54:59 GMT
- Sender: daemon@net.bio.net
- Distribution: bionet
- Lines: 31
-
- 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.
-
- Please reply to the neuroscience@net.bio.net list or email me
- directly, as my site doesn't receive every bionet.neuroscience posting
- for some reason.
-
- Thanks
-
- John
- -------
- John E. Anderson
- W. M. Keck Structural Biology Laboratory
- Cold Spring Harbor Laboratory
-