{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T04:58:31Z","timestamp":1789880311555,"version":"4.0.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurophysiology"],"published-print":{"date-parts":[[1996,11,1]]},"abstract":"<jats:p> 1. The black widow spider venom component, alpha-latrotoxin (alpha-LTx) (&lt; 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 Ca(2+)-free\/ethylene glycol-bis(b-aminoethyl ether)-N,N,N',N'-tetraacetic acid-containing saline, 100 microM Cd2+, or 50 microM 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\u20132.5 microM) 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 Ca(2+)-dependent, tetrodotoxin-sensitive spontaneous EPSCs, but did not affect evoked EPSC amplitude. 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 or evoked transmitter release in the hippocampus. 7. Potential presynaptic mechanisms that 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. <\/jats:p>","DOI":"10.1152\/jn.1996.76.5.3149","type":"journal-article","created":{"date-parts":[[2017,12,24]],"date-time":"2017-12-24T19:28:28Z","timestamp":1514143708000},"page":"3149-3158","source":"Crossref","is-referenced-by-count":73,"title":["Calcium-independent actions of alpha-latrotoxin on spontaneous and evoked synaptic transmission in the hippocampus"],"prefix":"10.1152","volume":"76","author":[{"given":"M.","family":"Capogna","sequence":"first","affiliation":[{"name":"Brain Research Institute, University of Zurich, Switzerland. capogna@hifo.unizh.ch"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B. H.","family":"Gahwiler","sequence":"additional","affiliation":[{"name":"Brain Research Institute, University of Zurich, Switzerland. capogna@hifo.unizh.ch"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S. M.","family":"Thompson","sequence":"additional","affiliation":[{"name":"Brain Research Institute, University of Zurich, Switzerland. capogna@hifo.unizh.ch"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"24","container-title":["Journal of Neurophysiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/jn.1996.76.5.3149","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T01:30:37Z","timestamp":1567992637000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/jn.1996.76.5.3149"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1996,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1996,11,1]]}},"alternative-id":["10.1152\/jn.1996.76.5.3149"],"URL":"https:\/\/doi.org\/10.1152\/jn.1996.76.5.3149","relation":{},"ISSN":["0022-3077","1522-1598"],"issn-type":[{"value":"0022-3077","type":"print"},{"value":"1522-1598","type":"electronic"}],"subject":[],"published":{"date-parts":[[1996,11,1]]}}}