Abstract
USE of purified snake venom neurotoxins with potent curarimimetic action on peripheral cholinergic transmission (for example, α-bungarotoxin1) in the study of the biochemical properties of the nicotinic cholinoceptor has met with considerable success (see ref. 2 for review). Some of the crude venoms from which such toxins have been isolated also contain toxins which act presynaptically, such as β-bungarotoxin1, notexin3 and taipoxin4. These three toxins inhibit the release of acetylcholine by a mechanism which is independent of the release process per se3–7. We show here that in an in vitro membrane preparation8 derived from the cholinergic endings in Torpedo electric organ these and related toxins are potent inhibitors of the high-affinity choline transport system. These observations provide a biochemical explanation for the inhibitory action of these toxins on transmitter release as they effectively block re-synthesis of acetylcholine from choline.
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DOWDALL, M., FOHLMAN, J. & EAKER, D. Inhibition of high-affinity choline transport in peripheral cholinergic endings by presynaptic snake venom neurotoxins. Nature 269, 700–702 (1977). https://doi.org/10.1038/269700a0
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DOI: https://doi.org/10.1038/269700a0
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