Lunesta shares its mechanism of action with the benzodiazepenes - Valium, Rohypnol, Xanax, etc. It doesn't actually belong to the benzodiazepene class of drugs, but they all work on the same system - GABA. Not coincidentally, the much-maligned GHB works by virtue of the fact that it is metabolized to GABA in vivo.
Lunesta belongs to a class of drugs that work similarly to benzodiazepenes but in such a way that they have a lower (but still nonzero) potential for abuse and dependency.
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Some time ago I just put together (with no input form myself) a post with all the information about it in one place. That post is to this day one of the most popular on the old Circadiana blog (though searches, mostly).
Is it just me or is that something a chemist would not want to put in his mouth? 4-methyl-2-aminopyridine has cardiac adrenergic effects.
So eszopiclone is a pretty damned good sedative/hypnotic, but with very little anxiolytic effect. I believe that's why it has less potential for abuse. BUT, it's metabolite N-desmethyl-(S)-zopiclone actually works at different subunits of the GABAa receptor, making it a pretty effective anxiolytic but not such a great sedative. I think a blind taste test of zop- and desmethylzop- is in order!
I am pretty sure that GHB is not metabolized to GABA, it is mearly an analog
I admit to some ignorance on this, but a quick medline search returns a recent article that at least partially supports the assertion.
I'm glad to be corrected on this (and I can't recall a citation to where I learned this, even a textbook) - anyone, please let me know if you can clear this up.
I took a pharma class and I asked if GHB was a GABA agonist, and the professor said that surprisingly, it is not a direct agonist (mimic of GABA). I'm not sure how it works though....
what does it mean if it keeps the patient up longer than before and acts more as a stimulant than a sedative?