Activity-Dependent Potentiation Of Synaptic Transmission From L30
Inhibitory Interneurons Of Aplysia Depends Upon Residual Presynaptic Calcium
But Not On Postsynaptic Calcium
Thomas M. Fischer, Robert S. Zucker, and Thomas J. Carew
Department of Psychology, Yale University, New Haven, CT 06520, Department
of Molecular and Cell Biology, University of California, Berkeley, CA 94720
APStracts 4:0085N, 1997.
ABSTRACT
Activity-induced short term synaptic enhancement (STE) is a common property of
neurons, one which can endow neural circuits with the capacity for rapid and
flexible information processing. Evidence from a variety of systems indicates
that the expression of STE depends largely upon the action of residual Ca2+
which enters the presynaptic terminal during activity. We have previously
shown that a Ca2+ -dependent STE in the inhibitory synapse between
interneurons L30 and L29 in the abdominal ganglion of Aplysia californica has
a functional role in regulating the gain of the siphon withdrawal circuit
through facilitated recurrent inhibition onto the L29s. In the present paper,
we further explore the role of Ca2+ in L30 STE by examining two basic issues:
(1) What is the role of residual presynaptic Ca2+ in the maintenance of L30
STE? We examine this question by first inducing STE in the L30s, then rapidly
buffering presynaptic free calcium through the use of the photo-activated Ca2+ chelator diazo-4, which was pre-loaded into the L30 neurons. Three forms of
STE in the L30s were examined; frequency facilitation (FF), augmentation
(AUG), and posttetanic potentiation (PTP). In each case, the activation-
induced enhancement of the L30 to L29 synapse was reduced to pre-activation
levels at the first test pulse following photolysis of diazo-4.
(2) What is the role of postsynaptic Ca2+ in the induction of L30 STE? We
examine whether there is a postsynaptic requirement of elevated Ca2+ for the
induction of L30 STE by first injecting the calcium chelator BAPTA into the
postsynaptic cell L29 (at levels sufficient to block transmitter release from
the L29s), in order to prevent any increase in postsynaptic intracellular Ca2+ which may occur during L30 (presynaptic) activation. We found that BAPTA
injection did not effect either the induction or the time course of FF, AUG,
or PTP in the L30s.
Taken collectively, our data indicate that all forms of STE in the L30s depend
upon presynaptic free cytosolic Ca2+ for their maintenance; but do not require
the elevation of postsynaptic Ca2+ for their induction.
Received 13 March 1997; accepted in final form 12 June 1997.
APS Manuscript Number J221-7.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 15 July 1997