Before I did a couple of searches on this today, I'd never seen anything really addressing the mechanism by which Mg2+ inhibits neuromuscular transmission. But this shows a direct blocking effect on nicotonic ACh receptor (nAChR) channels (a direct, anticholinergic effect that would be a postsynaptic action, as opposed to being a presynaptic inhibition of ACh release):
http://jp.physoc.org/cgi/content/abstract/443/1/683?ijkey=df962793a2b4db5f6cce5c2df3863e9ad6e76405&keytype2=tf_ipsecsha
(pubmed: http://www.ncbi.nlm.nih.gov/pubmed/1726594?dopt=Abstract)
It's possible that those concentrations are somewhat close to intracellular concentrations of magnesium that would be reached after an intravenous magnesium treatment. Here's another one showing basically the same thing:
http://www.ncbi.nlm.nih.gov/pubmed/1978344?dopt=Abstract
The researchers, the authors of both articles, found that intracellular Mg2+ was more potent in blocking the nAChR channels than extracellular Mg2+. Wait...The authors say that the reverse is true at the neuromuscular junction, that Mg2+ would act more extracellularly in that case. That's interesting. It's also interesting because the usual explanation, in all the articles, is that Mg2+ acts presynaptically to inhibit ACh release and doesn't bind to postsynaptic ACh receptors. There could still be an effect of Mg2+ on calcium channels, etc., though, even if this channel-blocking effect at nAChRs is meaningful in vivo.
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