DA rebound? what exactly do you mean?
Suppression of dopamine release due toGABAb agonism resulting in DA release once it ceases to block DA release?
What is the mechanism for this, anybody know? is it via something like stimulation of DA autoreceptors? it certainly doesn't feel, in vivo, like it is blocking transporters and thus acting as a reuptake inhibitor, otherwise, would we not be seeing stimulant properties? Which was certainly not the effect I got from taking phenibut.
As far as baclofen, if its alright my going slightly off on a tangent here, I've read recently (wikipedia), that the responses to baclofen can show some rather odd properties, depending on the user-some users of intrathecal baclofen to treat spasticity find that it is completely without effect via the intraspinal delivery route, yet find oral baclofen to be perfectly effective, yet some people get no, or almost no effect whatsoever from oral baclofen; no matter what the dosage used might get brought up to be but find intraspinal dosing via an implanted pump to do the trick.
That some might find it utterly useless per os is understandable enough, paradoxical rxns to some drugs are by no means unknown, I feel like shite for instance, if I take oxazepam, and benzos that metabolize to it later can, but don't always, make me shake, cause tremors and insomnia, APAP, for me, is completely and totally inert with regards analgesia, even given via IV infusion. But its unusual seeming that some people find baclofen useless intrathecally while still finding it works orally perfectly fine.
I've never tried it intraspinally, don't want to either, but even at doses of 200mg+ by mouth, or rectally it is more or less completely without action.
