Different components of black widow spider venom mediate transmitter release at vertebrate and lobster neuromuscular junctions

Abstract

Crude black widow spider venom (BWSV) has profound physiological effects on several neuromuscular preparations, both vertebrate and invertebrate¹. At frog and mouse neuromuscular junctions (NMJs), BWSV causes a massive increase in the frequency of miniature endplate potentials (m.e.p.ps)^2,3 followed by a reduction in m.e.p.p. frequency and depletion of synaptic vesicles^3–5. Qualitatively similar physiological and morphological effects are also observed at lobster^6–8 and insect^9,10 NMJs after treatment with BWSV. Apparently, therefore, this venom can cause the release of several transmitters—acetylcholine at vertebrate NMJs and γ-aminobutyric acid (GABA) and glutamate at invertebrate NMJs¹¹. BWSV has also been shown to cause the release of acetylcholine, noradrenaline and GABA from slices of mouse cerebral cortex^12,13. α-Latrotoxin, a protein of molecular weight (MW) 130,000, had previously been shown to be responsible for the venom effects at vertebrate NMJs and in mouse brain slices^12–14. That finding prompted the question of whether α-latrotoxin was also responsible for transmitter release in the lobster preparation. The present report demonstrates that although the electrophysicological effects of BWSV on lobster and frog NMJs are similar, they are caused by different components of the venom. The effects on the lobster are attributable to fraction E, which contains a major 65,000-MW protein and several lower molecular weight species. It has previously been shown that fraction E causes firing of the crayfish stretch receptor¹⁴. Some of these results have been published elsewhere¹⁵.