Activation of the Cannabinoid type 2 receptor causes the creation of new Mu Opioid receptors! It boosts the transcription of the gene that encodes the Mu receptors. This means CB2 agonists boost the level of mu receptors, and will boost a person's sensitivity to Mu agonists. 

could out of all the rc's coming out some be found to greatly increase the already enjoyable effects of opiates?  the paper specifically mentions jwh-15? Could you theoretically cause a person to have more mu opiod receptors than they normally would have?

Please list source for your comment, as it appears you discovered this , but here is the place where this comment was found ....

hxxp://herbs.maxforum.org/2012/03/20/cb2-agonists-induce-creation-of-new-mu-opioid-rece/



heres the paper link could have sworn it was attached hxxp://molpharm.aspetjournals.org/content/69/4/1486.full

split the part I found (top part from guy named toastus) with my question (bottom)

Reference Information


Cannabinoid Receptor Type 2 Agonists Induce Transcription of the ?-Opioid Receptor Gene in Jurkat T Cells
Christine Börner, Volker Höllt and Jürgen Kraus
Pharmacology
April 2006 vol. 69 no. 4 1486-1491




Abstract
Opioids and cannabinoids are both associated with analgetic, psychotropic, and immunomodulatory effects. It has been suggested that both systems interact on multiple levels. We hypothesized that cannabinoids induce opioid receptors and investigated cannabinoid-dependent expression of the ?-opioid receptor subtype in a human T cell model. We report that activation of the peripheral cannabinoid receptor type 2 leads to a de novo induction of ?-opioid receptor transcription in Jurkat E6.1 cells. We show that interleukin-4 is transcriptionally induced in response to cannabinoids and that an interleukin-4 receptor antagonist blocks cannabinoid-dependent induction of ?-opioid receptors, indicating that induced expression of interleukin-4 is required in this process. Induction of interleukin-4 is blocked by decoy oligonucleotides directed against STAT5, indicating the requirement of this transcription factor. In addition, we show cannabinoid-dependent phosphorylation of STAT5. Further experiments demonstrate that interleukin-4 then induces phosphorylation of STAT6, which directly transactivates the ?-opioid receptor gene. In addition, STAT6 induces expression of the transcription factor GATA3, which also contributes to ?-opioid receptor gene transcription. The responsive promoter region of the human ?-opioid receptor gene with the binding sites for both factors was mapped to nt -1001 to -950. To demonstrate functional ?-opioid receptor proteins, morphine-mediated phosphorylation of mitogen-activated protein kinase was investigated. We show that phosphorylation of mitogen-activated protein kinase occurs only in cannabinoid-prestimulated Jurkat E6.1 cells and that it is blocked by the ?-opioid receptor antagonist d-Phe-Cys-Tyr-d-Trp-Orn-Thr-Pen-Thr-NH2. In summary, these findings provide a first example for cannabinoid-opioid-interactions in cells of the immune system.

Even the abstract suggests that the IL4 antagonist will prevent the overgeneration of new opoid receptors. I think that the T cells were chosen to investigate the immune aspect of this... when I have had a strong coffee and finished the paper I will update this but they don't even seem to be looking at neurons.

The JWH molecules are a long way away from cannabis too...

yes extraordinary stuff aka anadamide   http://en.wikipedia.org/wiki/Anandamide