Oh yeah, it's actually one of the main things they do; it's one of their major roles in addiction. Lots of dopamine release upregulates kappa-opioid receptors causing levels to chronically drop in the absence of the drug stimulus and cause aversion, and waiting out the effects of dynorphin activating and downregulating those receptors during withdrawal is necessary to allow dopamine function to return. Though, on the other hand, animal data suggests that the process can be expedited by kappa-opioid agonists like salvinorin A, which by the way also tends to actually cause a euphoric afterglow even after its dysphoric trip, sort of like the opposite of a crash. When done at the peak of a psychedelic trip, I have also found it to cause a long-lasting dramatic increase of dream-like hallucinogenic effects and euphoria.
Interestingly, salvinorin A actually causes dopamine release in low to moderate concentrations that correspond to the doses that it can be more easily enjoyed at, but those huge dose terror trips you always hear about seem to lower dopamine across the board in animals. And those are also the ones that enhance my psychedelic trips for the longest.... Luckily when mixing it with psychedelics I also find it does go from dysphoric to mostly just not that euphoric, so that is nice, and that's part of what lead to my feelings about 4-HO-DET as well. So, when you describe DPT like that I would have to say it does sound like what I would expect, and an adrenaline-like feeling also corresponds quite well to what I get from high doses of salvia with psychedelics or without.... Definitely very fascinating, thanks for sharing that too.
I think we're on the verge of discovering some very intriguing new sides to all of our favorite drugs soon with all this new scientific research that's being done on them.
I imagine it's probably good to have some kind of self-regulation more so for tryptamines anyway just because they can mess with your mind so much.
