AMPLIFICATION OF SYNAPTIC CURRENT BY PERSISTENT SODIUM CONDUCTANCE IN
APICAL DENDRITE OF NEOCORTICAL NEURONS.
Schwindt, Peter C. and Wayne E. Crill.
Department of Physiology and Biophysics, Box 357290, University of
Washington School of Medicine, Seattle, WA 98195-7290.
APStracts 2:0279N, 1995.
SUMMARY AND CONCLUSIONS
1. Evidence for amplification of synaptic current by voltage-gated channels in
dendrites of neocortical pyramidal neurons was demonstrated by examining the
effect of specific channel blocking agents on the current arriving at the soma
during iontophoresis of glutamate at a distal site on the apical dendrite. 2.
Dendritic noninactivating Na+ channels were implicated in this voltage-
dependent amplification of the transmitted current because it was maintained
for greater than 1s and because tetrodotoxin (TTX) eliminated much of this
amplification . 3. Specific blockers of NMDA glutamate receptors reduced the
amplitude of the glutamate- evoked current at all potentials and also reduced
the non-TTX sensitive component of voltage- dependent augmentation. The
effects of TTX were identical whether or not NMDA channels were blocked. 4. We
conclude that a persistent Na+ conductance exists in the apical dendrite of
neocortical neurons. Together with the NMDA conductance at the synaptic site
it provides a mechanism for the graded, voltage-dependent amplification of
tonic, excitatory synaptic input. This amplification results in much more
effective transmission of tonic excitatory current to the soma than would
occur in a passive dendrite.
Received 17 July 1995; accepted in final form 29 August 1995.
APS Manuscript Number J452-5.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 September 1995.