Mamba Snake Venom

Abstract Mamba snake venom (Dendroaspis angusticeps, polylepis, viridis, jamesoni) contains a mixture of neurotoxic compounds including postsynaptic a-neurotoxins, dendrotoxins, fasciculins, and muscarinic toxins (2). Effects at the neuromuscular junction include acetylcholinesterase inhibition (fasciculins) and increased presynaptic release of ace tylcholine (dendrotoxins); together with the high acetylcho line content of mamba toxin (6-24 mg/g), these effects are synergistic and enhance neurotoxicity and lethality (4,5). Some of these toxins are discussed elsewhere (see Fascicu lins, Dendrotoxin, this volume). Toxins that facilitate neuromuscular transmission are a characteristic component of mamba venom. The four known fasciculins (see Fasciculins, this volume) bind to a peripheral regulatory anionic site of acetylcholinesterase in a noncompetitive and irreversible manner (2). The dendrotoxins comprise the second group of facilitatory neurotoxins and are present in most mamba venoms (with the exception of Dendroaspis jamesoni ); they inhibit voltagedependent K+ channels in motor nerve terminals and facilitate acetylcholine release at the neuromuscular junction (2,5). Postsynaptic toxins present in mamba venom bind to and block nicotinic acetylcholine receptors. The muscarinic toxins present in mamba venom are small (7 kDa) proteins that selectively bind to muscarinic cholinergic receptors and may constitute up to 1 % of the venom protein (1,3).