mkirby at vt.edu (Mike Kirby) writes:
>eleusis at netcom.com (Eleusis) wrote:
> > The best theory going, AFAIK, is that alcohol causes generalized neuronal
> > membrane depolarization in much the same way that anesthetics work, except
> > anesthetics do it with a bit more selectivity.
> What exactly is AFAIK? This not a term that I've encountered before in
> the pharmacological or toxicological literature. As for EtOH mode of
(a)s (f)ar (a)s (I) (k)now
Editors of probably all of the better pharmological, medical, etc
journals tend to frown on these types of abbrvs... usenet doesnt.
> action, EtOH IS classified as a GABA-A agonist and not characterized as a
> having properties similar to anesthetics. Anesthetics, which I assume
> from your description you're referring to locals, tend to cause block in
> voltage-gated Na+ channels and also have effects on voltage-dependent,
> non-inactivating Na+ conductances. This differs signifcantly from the
> effects EtOH imposes on neurons. Where did you get your information? If
> there is tenable evidence for other modes of action for EtOH, I'd like to
EtOH is one of those esteemed "multi-action" drugs. Remember the
tricyclic antidepressants? Not only did they block 5HT and NE reuptake,
they also blocked lots of other stuff... which is why they were so
"inneffective". (Apparently tricyclics are often more effective than
SSRIs, but who wants to take a tricyclic with all the side effects..)
Ethanol isnt just a GABA-ergic drug... consider the sheer volume of the
stuff consumer... it effects EVERYTHING. In fact, if the persons also all
coked up, it actually makes a third drug (cocaethylene) right in the
persons body... basically due to the amount of ethanol, there's most
likely an endless variety of modes of action...
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