primary afferent depolarization

John Anderson anderson at CSHL.ORG
Mon Jan 25 07:54:59 EST 1993

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

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 at net.bio.net list or email me
directly, as my site doesn't receive every bionet.neuroscience posting
for some reason.


John E. Anderson
W. M. Keck Structural Biology Laboratory
Cold Spring Harbor Laboratory

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