The effects of black widow spider venom (BWSV) on the crayfish stretch receptor and the lobster neuromuscular junction were examined. In crayfish stretch receptor neurons, BWSV caused a slight hyperpolarization followed by a large depolarization. The venom-induced depolarization of the stretch receptor was caused by an increase in membrane conductance to Na+ and Ca2+. Black widow spider venom also caused an increase in the frequency of miniature inhibitory postsynaptic potentials recorded in the stretch receptor. The ability of BWSV to increase the frequency of miniature excitatory postsynaptic potentials (MEPSPs) at the lobster neuromuscular junction was dependent on the divalent cation composition of the bathing medium. Ringer solutions containing Ca2+ supported the greatest venom-induced increase in MEPSP frequency, Mg2+ and Mn2+ supported a moderate increase in MEPSP frequency, while Co2+ and Zn2+ blocked this venom effect entirely. Black widow spider venom did not block axonal conduction in lobster walking leg axons or in the axon of the crayfish stretch receptor. The results suggest that in crustaceans, BWSV interacts specifically with membrane of the soma-dendritic region of the stretch receptor and with nerve terminal membrane, causing an increase in Na+ and Ca2+ conductance.