Interaction Between Opioids and Salvia?

[RhythmSpring]

I just had an intriguing experience. I have been coming off of percocets for pain from a recent elbow surgery, and I smoked some 13x Salvia. I hadn't ingested percocet for about 24 hours. As a regular Salvia smoker, this experience was markedly different from all my other ones. It was much more euphoric, and had a pleasant head-rush. It was very relaxing, particularly mentally relaxing. I was still able to gain profound insight from the experience, too. It was one of the strongest trips on Salvia I've done, especially considering the amount I used.

My face remains pleasantly warm and flushed. I was able to access some hidden memories and some deep underlying thought patterns that I have been neglecting.

Since both oxycodone and Salvia affect the opioid systems, is there any possibility of any kind of synergy between the two?

[By the way, I posted a thread a couple weeks ago asking about possible interactions between various drugs that affect the opioid receptors, and it was immediately laughed at and closed. ...That was dumb. Proof above. Also, proof in the fact that Iboga and opiates should NOT be mixed, which were two of the substances I asked about in the previous thread.]

 

[Cyb]

I'm most certainly not qualified to be posting in ADD, but -
Salvinorin is a Kappa agonist. This means it does indeed affect the opioid system of the body but not in the ways one would expect. Typically kappa agonism is dysphoric - in fact, the ''antidepressive'' effects of Burprenorphine are attributed to its kappa ANTagonism. \

Regarding synergism between the two... yes, there could be some, but AFAIK oxycodone is not a profound K agonist, as most opioids, therefore I would not consider dual administration to be a problem.

 

[adder]

Kappa agonism is considered dysphoric but I'd rather describe it as sedative in a dull way and psychomimetic in the first place (and well, these effects actually make KOR agonists dysphoric). Salvinorin A has a strong affinity at KOR, oxycodone is rather weak there (cf. morphine balanced action at opioid receptors, if God exists, he/she must have had it in mind to make it so good ). Besides salvinorin A also affects dopamine in some way, look up researches, they've been done. As this is a psychedelic/hallucinogen, I won't pretend to be an expert here but there's definitely some synergy but not to such an extent that salvinorin A would really boost up oxycodone. It's rather a result of conjoint action of oxycodone and salvinorin A. It's not like you took some shitty racemic pentazocine activating both KOR and sigma receptors.

And concerning buprenorphine's antidepressant action, kappa antagonism definitely plays a major role but it's not really fully understood how depression is counteracted. There are so many kappa antagonists and they never made it to be used as antidepressants. But here I've got my own opinion why opioids aren't used, big pharmaceutical companies make just too much money from their shitty "antidepressants" which action is rather a temporary solution. Whether you suffer mentally or physically it's actually the same so basically all opioids can be called antidepressants. Buprenorphine is just safer because it's a partial MOR agonist and it's still enough to release serotonin and dopamine. Something partially MOR activating, kappa blocking, NMDA blocking with some little sigma activity is a way to go; it all guarantees release of neurotransmitters helping in depression. Really, I got sick of these 5-HT and/or NA, and/or DA transporter(s) blockers long time ago. Never really helped me for good. Buprenorphine did a good job but it was too weak to fight my withdrawals when tapering down. Whoa!...

 

[ebola?]

How well known is the biology of the interaction between different types of opioid activation? Does kappa agonism moderate tolerance accrual via mu and perhaps delta agonism? If so, what would this indicate about small-timescale effects of cells with mu or delta opioid receptors?
...
Insofar as salvia binds at kappa with much greater affinity than wide-spectrum opioid ligands, it should increase effect at other opioid sites (as, they will bind elsewhere).

ebola

 

[sekio]

How well known is the biology of the interaction between different types of opioid activation?

As far as I know (and I'm no expert) the "five pathways" of mu, delta, kappa, sigma and NMDA are totally seperate. It's mere coincidence that the ligands, natural and otherwise, share affinities.

I think the mu and delta pathways are the "closest" to each other; kappa is still "in the family" so to speak but it has a much different action than mu/delta, and the sigma receptors are only considered opioid receptors if you subscribe to the now-antiquated model of thought. The NMDA receptor is also related and many opiods share activity there (methadone, the *azocines). The azocines are really the most promiscuous with the epoxymorphinans being the most specific for mu/delta.

From what I know the three engogenous ligands (mu - endorphin, delta - enkephalin, kappa - dynorphin) each have an affinity for their one receptor but also are capable of activating receptors not "in their court" - just not as well as the "native" peptides. the sigma and NMDA receptors are not "true opioid" receptors and are not activated by e.g endorphin, only exogenous ligands.

The kappa opioid receptor is quite puzzling indeed. Given that there are few things as strongly activating of the KOR as salvia I would say that you just lucked out. Even oxycodone etc don't provide appreciable effects at KOR.

 

[RhythmSpring]

Hmmm, perhaps I will repeat the experiment closer to the time I've ingested an opioid. I could also try it while on kratom, to see if there's any kind of mu-kappa interaction. I tell ya, the afterglow from this one Salvia trip is the strongest I've ever felt from a Salvia trip.