INHIBITION OF DENDRITIC CALCIUM INFLUX BY ACTIVATION OF G-PROTEIN-COUPLED
RECEPTORS IN THE HIPPOCAMPUS.
Huanmian Chen and Nevin A. Lambert.
Department of Pharmacology and Toxicology, Medical College of Georgia and
Veterans Affairs Medical Center, Augusta, Georgia.
APStracts 4:234N, 1997.
ABSTRACT
Gi proteins inhibit voltage-gated calcium channels and activate inwardly-
rectifying K+ channels in hippocampal pyramidal neurons. The effect of
activation of G-protein-coupled receptors on action potential-evoked calcium
influx was examined in pyramidal neuron dendrites using optical and
extracellular voltage recording. We tested the hypotheses that: 1) activation
of these receptors would inhibit calcium channels in dendrites, 2)
hyperpolarization resulting from K+ channel activation would deinactivate low-
threshold, T-type calcium channels on dendrites, increasing calcium influx
mediated by these channels, and 3) activation of these receptors would inhibit
propagation of action potentials into dendrites, and thus indirectly decrease
calcium influx. Activation of adenosine receptors, which couple to Gi
proteins, inhibited calcium influx in cell bodies and proximal dendrites
without inhibiting action potential propagation into the proximal dendrites.
Inhibition of dendritic calcium influx was not changed in the presence of 50æM
nickel, which preferentially blocks T-type channels, suggesting influx through
these channels is not increased by activation of G-proteins. Adenosine
inhibited propagation of action potentials into the distal branches of
pyramidal neuron dendrites, leading to a 3-4 fold greater inhibition of
calcium influx in the distal dendrites than in the soma or proximal dendrites.
These results suggest that voltage-gated calcium channels are inhibited in
pyramidal neuron dendrites, as they are in cell bodies and terminals, and that
G-protein-mediated inhibition of action potential propagation can contribute
substantially to inhibition of dendritic calcium influx.
Received 19 June 1997; accepted in final form 9 September 1997.
APS Manuscript Number J504-7.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 7 October 1997