Abstract
The effects of the crude venom of the Australian common brown snake on the mammalian neuromuscular system have been investigated. The venom was injected subcutaneously into the dorso‐lateral aspect of one hind limb of the rat. The limb was paralysed within 90 min and remained paralysed for 2 to 3 days. The exposed muscles failed to respond to indirect excitation, and individual fibres were not depolarized at the nerve‐muscle junction by exposure to carbachol. The wet weight, histological appearance, resting potential and input resistance of the muscle fibres and their ability to generate directly elicited action potentials were unaffected by exposure to the venom. Administration of venom to isolated preparations caused a reduction in the amplitude of miniature endplate potentials, with no change in frequency. The quantal content of evoked endplate potentials was unchanged. It was concluded that the crude venom was largely devoid of presynaptic activity and myotoxicity, and that its primary site of neurotoxicity was directed to the postsynaptic membrane.