The Journal of Neurophysiology Vol. 78 No. 4 October 1997, pp. 2061-2071
Copyright ©1997 The American Physiological Society

Activity-Dependent Potentiation of Synaptic Transmission From L30 Inhibitory Interneurons of Aplysia Depends on Residual Presynaptic Ca²⁺ But Not on Postsynaptic Ca²⁺

Thomas M. Fischer¹, Robert S. Zucker², and Thomas J. Carew¹

¹ Department of Psychology, Yale University, New Haven, Connecticut 06520; and ² Department of Molecular and Cell Biology, University of California, Berkeley, California 94720

Fischer, Thomas M., Robert S. Zucker, and Thomas J. Carew. Activity-dependent potentiation of synaptic transmission from L30 inhibitory interneurons of Aplysia depends on residual presynaptic Ca²⁺ but not on postsynaptic Ca²⁺. J. Neurophysiol. 78: 2061-2071, 1997. Activity-induced short-term synaptic enhancement (STE) is a common property of neurons, one that 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 on the action of residual Ca²⁺, which enters the presynaptic terminal during activity. We have shown previously 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 photoactivated Ca²⁺ chelator diazo-4, which was preloaded 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 preactivation 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 bis-(o-aminophenoxy)-N,N,N,N-tetraacetic acid (BAPTA) into the postsynaptic cell L29 (at levels sufficient to block transmitter release from the L29s), to prevent any increase in postsynaptic intracellular Ca²⁺ that 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 on presynaptic free cytosolic Ca²⁺ for their maintenance but do not require the elevation of postsynaptic Ca²⁺ for their induction.

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