alpha-latrotoxin of black widow spider venom depolarizes the plasma membrane, induces massive calcium influx, and stimulates transmitter release in guinea pig brain synaptosomes.

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Abstract
The effect of .alpha.-latrotoxin from black widow spider venom upon guinea pig cerebral cortical synaptosomes was described. Plasma membrane potential (.DELTA..psi.p), in situ mitochondrial membrane potential (.DELTA..psi.m), Ca2+ transport, .gamma.-amino[3H]butyrate release, [3H]noradrenaline [norepinephrine] release and synaptosomal ATP were monitored under parallel conditions. Potentials were determined isotopically and with a tetraphenylphosphonium-selective electrode. .alpha.-Latrotoxin depolarized .DELTA..psi.p selectively, in the presence and absence of Ca2+. A slight toxin-induced depolarization of .DELTA..psi.m was a consequence of a massive Ca2+ uptake across the plasma membrane. Depolarization of .DELTA..psi.p was insensitive to tetrodotoxin, and Ca2+ entry was only partially inhibited by verapamil. Release of [3H]noradrenaline and .gamma.-amino[3H]butyrate was markedly stimulated by the toxin in the presence of Ca2+, and this effect was only slightly reduced in Ca2+-free conditions.

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