He says "O-4394 and O-4395 exhibit similar in vitro potencies to eDelta(9)-THCV as CB(1) receptor ligands and as antagonists of cannabinoid receptor agonists and can antagonize Delta(9)-tetrahydrocannabinol in vivo."

But what I get from that is these opioids act as THC agonists and block the action of other cannabinoid agonists. This does not answer his question.

I would think that the opposite would occur in that having both THC and tramadal would increase the rate and production of MAO and COMT, enzymes which break down many types of neurotransmitters. This would in fact decrease the amount of neurotransmitters making it to receptors after your blood THC/Tramadal levels are low enough.

This suggests that enzymes are not at work. Perhaps the down regulation of cannabinoid receptors, which has been shown to happen after being exposed to large(ish) amounts of cannabinoids, causes an increase in sensitivity to Tramadal?
partcleguy Reviewed by partcleguy on . Wondering about a particular effect of THC on the MU1 receptor-agonist mechanisms Last night I was in a significantly extra large amount pain so I took an extra dose of tramadol (a morphine receptor agonist), and now I've woken up at 3:00am with seratonin blasting through my brain. I'm unable to sleep because my brain is utterly excited, eccentric and wildly creative in thought, enthusiastic and possitive in outlook (as opposed to the usual as of late), and overal very clear thinking. I attribute this to the increase and reuptake-inhibition of seratonin triggered by tramadol Rating: 5