MODIFICATION OF THE TRANSMISSION OF SYNAPTIC CURRENT BY BLOCKADE OF
VOLTAGE- AND Ca2+-DEPENDENT CONDUCTANCES IN APICAL DENDRITE OF RAT NEOCORTICAL
PYRAMIDAL NEURONS.
Peter C. Schwindt and Wayne E. Crill.
Department of Physiology & Biophysics, University of Washington School of
Medicine, Box 357290, Seattle, WA 98195-7290.
APStracts 4:0053N, 1997.
ABSTRACT
The tonic axial current transmitted from dendrite to soma was measured by
somatic voltage clamp during the long-lasting iontophoresis of glutamate at a
distal site on the apical dendrite of rat neocortical pyramidal neurons.
Evidence for voltage- and Ca2+-gated channels in the apical dendrite was
sought by examining the modification of this transmitted current resulting
from alteration of membrane potential and application of specific channel
blocking agents. When NMDA receptors were blocked, iontophoresis of glutamate
on the soma evoked a current whose amplitude decreased linearly as membrane
potential was decreased from -90 to -40 mV with an extrapolated reversal
potential near zero mV. Under the same conditions, glutamate iontophoresis at
sites on the apical dendrite 241 to 537 æm from the soma resulted in a
transmitted axial current that increased with depolarization over the same
range of membrane potential. Current transmitted from dendrite to soma was
thus amplified during somatic depolarization from resting potential (-70 mV)
and attenuated during hyperpolarization. After Ca2+ influx was blocked to
eliminate Ca2+-dependent K+ currents, application of 10 mM TEA altered the
amplitude and voltage dependence of the transmitted current in a manner
consistent with the reduction of dendritic voltage-gated K+ current. We
conclude that dendritic, TEA-sensitive, voltage-gated K+ channels can be
activated by tonic synaptic depolarization. The most prominent effects of
blocking Ca2+ influx on tonic transmitted current resembled those elicited by
TEA application, suggesting that these effects were caused predominantly by
blockade of a Ca2+-dependent K+ current. When cells were impaled with EGTA-
containing microelectrodes to prevent a rise in intracellular Ca2+
concentration, blockade of Ca2+ influx altered the tonic transmitted current
in different manner consistent with the blockade of a dendritic inward current
carried by high-threshold-activated Ca2+ channels. We conclude that the
primary effect of Ca2+ influx during tonic dendritic depolarization is the ac
tivation of a dendritic Ca2+-dependent K+ current. The hyperpolarizing
attenuation of transmitted current was unaffected by blocking all known
voltage-gated inward currents except Ih. Extracellular Cs+ (3mM) reversibly
abolished both the hyperpolarizing attenuation of transmitted current and Ih
measured at the soma. We conclude that activation of Ih by hyperpolarization
of the proximal apical dendrite would cause less synaptic current to arrive at
the soma from a distal site than in a passive dendrite. Several implications
of dendritic K+ and Ih channels are discussed.
Received 5 June 1996; accepted in final form 14 January 1997.
APS Manuscript Number J449-6.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 20 February 1997