"neuromuscular block" by binding to alpha-3 / alpha-4 subunit

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Neither of the two named subunits are part of the muscle-type nicotinic acetylcholine receptor, so the given statement in the article is confusing. According to scientific papers (see examples below), kappa-bungarotoxin does block vertebrate neuromuscular transmission but with a low potency. However it is much more effective at blocking neuronal nicotinic receptors, especially the ganglion-type receptor. In addition, it seems to be a common minor component of krait venom, with alpha-bungarotoxin often being the major component that causes paralysis and respiratory arrest (in vertebrates).

See e.g.:

https://www.researchgate.net/publication/17047462_Kappa-Bungarotoxin_a_probe_for_the_neuronal_nicotinic_receptor_in_the_avian_ciliary_ganglion

http://jeb.biologists.org/content/141/1/61

--79.240.206.102 (talk) 21:50, 19 September 2018 (UTC)Reply

You're right, that was obviously a mistake by the article's author (errm, that would be me) - the cited source even explicitly states as much. I believe you're right on the venom composition too - for sure that kappa is present at lower concentration than alpha in venom, though I didn't come up with relative toxicity on a quick search. Opabinia regalis (talk) 06:18, 30 September 2018 (UTC)Reply