Psycho-Babble Medication | about biological treatments | Framed
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Re: provigil discussion

Posted by tessellated on February 25, 2006, at 20:15:32

In reply to Re: provigil discussion, posted by zeugma on February 25, 2006, at 17:42:12

cool refs, like this serious kinda info.
now are alpha-2 sites presynaptic autoreceptors?
i did not believe this to be the case.
lemme spend time on the refs many thanks,

ps: antagonizing a presynaptic autoreceptor can result in an increase of NE release. as they modulate NE production; and can infact inhibit NE release/production if agonists/excess NE are present. An antagonist can have post synaptic agonistic affect. Get it? Stimulation can cause inhibition and vice versa.. It's freaking complex....

> I have to agree with SLS, Provigil is not an alpha-2 antagonist (antagonist of pre-synaptic NE autoreceptors). If that were the case then depleting an animal of norepinephrine would result in a loss of its effect (similar to the way depleting an individual whose depression has remitted on desipramine results in a relapse), but this seems not to be the case.
> On the other hand, animals that lacked dopamine transporters experienced no stimulating effect from either methamphetamine or Provigil, indicating that DA reuptake inhibition is involved. These animals were hypersensitive to caffeine, so it's safe to say that caffeine and Provigil do not share the same mechanisms.
> An experiment was also conducted in which Provigil's effect on the ventrolateral proptic nucleus (a major site of sleep regulation) and apparently Provigil blocked the NE transporters in that region:
> If Provigil does act as an NE transport blocker it must be extremely localized, because every other NE transport blocker inhibits cataplexy, and Provigil does not do so at all.
> The author who comments on the study I cited above theorizes that the combination of weak DA reuptake inhibition, and localized NE reuptake inhibition, may combine to produce its wakefulness effect. Provigil does release orexin, but it has no direct effect on that system (i.e. it is not a ligand for a known orexin receptor). Its effect on GABA inhibition is also well documented:
> These effects on GABA and norepinephrine are extremely localized and peculiar, at they seem so to me.
> -z




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