Why I don't believe the GHB dopamine rebound theory

[iconoclast56]

I genuinely have ADHD and amphetamines calm/tranquilize me. If I take GHB, when it wears off after about 4 hours I end up nervous and anxious. I can counteract this with amphetamines but I need to take more amps than I usually would. For 4 or so hours, the effects of the amphetamines are dulled. If these stimulatory aftereffects of GHB were caused by dopamine then their effects should combine with the effects of amphetamines, not cancel each other out. For now, I'm gonna go with the theory that the "dopamine rebound" is actually the effects produced by activation of the GHB receptor. I'd like to try a selective GHB agonist to see what effects it would have. I'm going to get some phenibut soon and will find out what effects the selective activation of GABA_B receptor produced.

 

[nuvanob]

I would actually be surprised if the sudden drop of gaba b agonism at the 4 hour mark of a GHB session didn't play a major part in the 'dopamine rebound' phase (disclaimer- I have no personal experience or scientific basis for that belief). That said, phenibut is a very mild drug that has nasty withdrawal effects if you take it regularly, so use caution in any experiments. I gotta say that your use of amphetamines to get through GHB comedowns sounds kinda dangerous to my layman sensibilities.

 

[atrollappears]

It could be that the excess dopamine is metabolized into noradrenaline by dopamine beta-hydroxylase, and that's what's giving you the nervous/anxious feeling.

 

[atrollappears]

^ Doesn't that happen with amphetamine too though?

Probably. Maybe that's why it doesn't work so well hahaha. But i could still see the frontocortical-dopamine sedation overcoming it if that's how his brain works out. And who knows, with alpha 2 autoreceptors and all...

 

[Drunk with Power]

This study suggests that activation of the GHB receptor increases extracellular glutamate, while activation of the GABA(B) receptor reduces glutamate. So when GHB's GABA(B) agonism decreases after a few hours, you'll end up with excess glutamate which explains the agitated sensation when GHB wears of. This probably explains the neuroadaptive changes in the NMDA receptor subunits in the hippocampus (and the cognitive deficits associated with chronic GHB abuse) as well. I hope this helps, I'm not a professional though.

http://www.ncbi.nlm.nih.gov/pubmed/14535954

 

[iconoclast56]

^ Doesn't that happen with amphetamine too though?

Weirdly enough, I often have to take high doses of amphetamines to counteract the side effects of lower doses of them. Maybe thats the explanation. Maybe its not dopamine that I need more of, maybe its norepinephrine.

 

[atrollappears]

Weirdly enough, I often have to take high doses of amphetamines to counteract the side effects of lower doses of them. Maybe thats the explanation. Maybe its not dopamine that I need more of, maybe its norepinephrine.

Probably the opposite, stims affect NE comparatively more at lower levels and DA comparatively more at higher levels. ADHD that responds to norepinephrine-type treatments is characterized by pure inattentive behavior, i.e. difficulty planning, organizing, and initiating tasks properly (and strangely enough often presents with hypertension), rather than maintaining them as with ADHD hyperactive (usually dopamine responsive). The former type often does not improve or gets worse with d-amphetamine treatment, while responding to things like strattera, intuniv, and lower doses of ritalin/adderall.