Presynaptic inhibition of calcium-dependent and -independent release elicited with ionomycin, gadolinium, and [alpha]-latrotoxin in the hippocampus. Capogna, Marco, Beat H. G[umlaut]ahwiler, 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: +41-1-385 65 04, E-mail: thompson @ hifo.unizh.ch .
APStracts 2:0323N, 1995.
SUMMARY AND CONCLUSIONS
1. Presynaptic inhibition of synaptic transmission in the hippocampus was investigated by comparing the effects of several agonists on miniature excitatory and inhibitory postsynaptic currents (mEPSCs and mIPSCs). 2. The Ca 2+ ionophore ionomycin increased the frequency of mEPSCs and mIPSCs, but did not affect their amplitude. Ionomycin-induced release required extracellular Ca 2+ and was prevented by pre-treatment with botulinum neurotoxin serotype F, like evoked synaptic transmission. Unlike evoked transmission, however, this increase did not involve activation of voltage-dependent Ca 2+ channels because it was insensitive to Cd 2+ . 3. Both the lanthanide gadolinium and [alpha] -latrotoxin produced increases in the frequency of mEPSCs and mIPSCs, but their actions were independent of extracellular Ca 2+ . 4. Adenosine, the GABA B receptor agonist baclofen, and a [mu] -opioid receptor agonist strongly reduced the frequency of synaptic currents triggered by all three secretagogues. 5. We conclude that activation of these presynaptic receptors can reduce high frequencies of vesicular glutamate and GABA release by directly impairing transmitter exocytosis. Presynaptic inhibition of gadolinium- and [alpha] -latrotoxin-induced release indicates that this impairment occurs without changes in intraterminal Ca 2+ homeostasis and when vesicle fusion is rendered Ca 2+ independent, respectively. 6. The inhibition of ionomycin-induced release provides additional evidence for a direct, neurotransmitter receptor-mediated modulation of the proteins underlying vesicular docking or fusion as an important component of presynaptic inhibition of evoked synaptic transmission. 

Received 1 September 1995; accepted in final form 30 October 1995.
APS Manuscript Number J582-5.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 November 95