Cb1 and KOR upregulation

[Turing Machine]

I'm hoping this is of an appropriately advanced level for this forum, if not, please move this to the correct forum.

I've read a few journal articles which discuss CB1 agonists upregulating Kappa Opioid Receptors (KOR) and KOR agonists upregulating CB1 receptors but I've been unable to relocate some of the better ones after losing them in the unrecoverable data on a crashed hard disc. I remember the one test performed in one article showing this effect was quite strong. If anyone knowledgeable on the subject, or at least more knowledgeable than me, could explain the extent of this mechanism with respect to how weak KOR agonists which possibly occur in herbal cannabis may modulate the effects of THC. I've smoked nearly pure THC and find it uninteresting and mild compared to relatively low resin heirloom narrow leafed >26 week flowering tropical varieties. A friend in Holland had provided me with pure THCV and CBD to prove to me that they have nothing approaching psychedelic effects. Could the relationship between CB1 receptors and KOR's be responsible for at least a percentage of how subjective potency of cannabis is able to differentiate itself from THC content? Would it be worthy to examine unusual terpenes present in highly visual and psychedelic long flowering tropical heirloom samples for weak KOR activity?

 

[onmyway]

thats an interesting idea. i suppose one could experiment with salvia, which i believe is psychoactive via a kappa agonist.

 

[Phener]

interesting so CB1 agonists upregulate Kappa opioid

maybe that is where the high THC linked to adolescence schizophrenia comes from, some KOR upregulation process

 

[Astavats]

Excuse me if I am over-stepping my boundary of understanding but when I read the title it reminded me of hearing about mGlu2/5-HT2A heterodimerized receptors. From what I understand, when mGlu2 receptor was activated 5-HT2A would be deactivated (or signals inhibited?) and vice versa. If KOR/CB1 follow this same concept it seems to make sense why it would upregulate the other receptor, it would act almost as a antagonist. Have I misunderstood something?

I found this article discussing what I'm suggesting, I haven't gone through it in complete yet.

"k-Opioid receptors and CB receptors might signal through a common G protein or form functional heterodimers, as recently described for mu-opioid and CB1 receptors"

 

[Coolio]

The CB1 receptor and the mu opioid receptor (MOR) are potential heterodimer receptors. Agonism at either receptor causes an allosteric interaction with the other receptor.