®MDNM¯Calcium-independent actions of [alpha] -latrotoxin on spontaneous and evoked synaptic transmission in the hippocampus. Marco Capogna, Beat H. Gahwiler, and Scott M. Thompson. Brain Research Institute, University of Zurich, August Forel-Strasse 1, CH- 8029 Zurich, Switzerland, Tel: +41-1-385 63 55, Fax: +41-1-422 22 62, E-mail: capogna @ hifo.unizh.ch.
APStracts 3:0147N, 1996.
SUMMARY AND CONCLUSIONS
1. The black widow spider venom component, [alpha] -latrotoxin ( [alpha] -LTx) (<0.5 ? nM), increased the frequency of miniature excitatory postsynaptic currents (mEPSCs) in hippocampal CA3 pyramidal cells 14-fold, without changing their amplitude. 2. This action of [alpha] -LTx was not affected by application of Ca2+-free/EGTA saline, 100 [mu] M Cd2+, or 50 ? [mu] M Gd3+. The increase in mEPSC frequency was thus not due to an influx of Ca2+ into the axon terminal via voltage-dependent Ca2+ channels or [alpha] -LTx-induced pores. 3. [alpha] -LTx did not increase spontaneous release when synaptic transmission had been impaired by botulinum toxin/F. 4. [alpha] -LTx reduced the amplitude of EPSCs, elicited with stimulation of mossy fibers, without affecting paired-pulse facilitation. 5. The Ca2+ ionophore ionomycin (2-2.5 [mu] M) also enhanced the frequency of mEPSCs, but unlike [alpha] -LTx, potentiated evoked EPSCs and reduced paired-pulse facilitation. Application of N -methyl- D -aspartate elicited a high frequency of Ca2+-dependent, TTX- sensitive spontaneous EPSCs, but did not affect evoked EPSC amplitudes. Agents that stimulate vesicular release by increasing presynaptic Ca2+ influx thus do not mimic the [alpha] -LTx-induced depression of evoked EPSCs. 6. We conclude that entry of Ca2+ into presynaptic axon terminals is not responsible for the effects of low concentrations of [alpha] -LTx on either spontaneous and evoked transmitter release in the hippocampus. 7. Potential presynaptic mechanisms which could mediate the opposing actions of [alpha] -LTx on spontaneous and evoked transmitter release in the hippocampus (i.e., [alpha] -LTx-induced ionic pores, depletion of synaptic vesicles, actions on exocytotic proteins) are discussed.

Received 29 April 1996; accepted in final form 27 June 1996.
APS Manuscript Number J351-6.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 25 July 1996