In article <mkirby-2503962014060001 at ntoxlab.ento.vt.edu> 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
Heheheh. As Far As I Know....
>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
No, this is advancing a model in which the ethanol partitions into the
lipids, as do many *general* anesthetics. The theory on generals (the
partition theory, that is) is that they may have relatively nonspecific
effects which first become manifest in neurons with smaller diameter
fibers and somata, if I'm remembering it correctly. An alternative is
that there are some lipid-accessible binding sites for the anesthetics,
by *very* broad analogy with batrachatoxin in voltage-dependent sodium
channels (which is to say, the EtOH binding sites can be thought to be
low-affinity sites on the GABA receptors which are primarily
lipid-accessible, if you'd like a Grand Unified Theory.)
There was a review of this in Science about 4-5 years ago, and I haven't
followed it too closely since then, so I'm likely misremembering the
details. There's also some discussion of this in Goodman and Gilman in
the discussion of general anesthetics and the introduction of ether.
Anyone know what the effective molar concentration of the "officially
intoxicated" EtOH blood level is? I'm thinking something in the range of
40 micromolar....
-=Peter
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