Well its all a very interesting area of research. Although im not
particularly awear of the articles you refer to. I imagine
nonpsychoactive cannabinoids protect from ischemic damage via their
antioxiditive properties, so vitamine E could be just as good.
What I meant by the MK-801 comment was not just limited to the
psychoactive side effects, but the fact that they have to be administered
very soon after the stroke, so their usefulness is very limited.
Don't get me wrong, the the in vitro studies arn't directly comparable to
recreational/clinical usages of cannabinoids, but they do point out a
need for caution. Also, you say that no neurtoxicity has been shown in
vivo with sensible doses. It depends on how you define sesnible doses, if
we account for the usual interspecies dosing changes, the doses given to
mice to produce "neurotoxicity" are not that outlandish.
...and of course, when I say neurotoxicity I mean the ICON definition, so
that include morphological changes, which CB1 agonists of varying kinds
As far as the Maccarrone et al article, its a rather interesting set or
research. Some peopl then ending up concluding that neither receptors had
anything to do with anadamide induced apoptosis, and it was a lipid raft
mediated phenomena. In reality, I suspect its a complex interplay. But of
course, THC dosn't activate the vanilloid receptor, so that whole
argumennt is rather peripheral to THC-mediated neurtoxicity.
and as far as cannabinoids recieving more attention, well if I can charm
my head of my department, THC/anandamide-mediated neurotoxicity is
hopefully what I'll do my masters on.