Cannabinoid receptors are activated by cannabinoids, generated naturally inside the body (=endocannabinoids) or introduced into the body as cannabis or a related synthetic compound.

After the receptor is engaged, multiple intracellular signal transduction pathways are activated. At first, it was thought that cannabinoid receptors mainly inhibited the enzyme adenylate cyclase (and thereby the production of the second messenger molecule cyclic AMP), and positively influenced inwardly rectifying potassium channels (=Kir or IRK)[7]. However, a much more complex picture has appeared in different cell types, implicating other potassium ion channels, calcium channels, protein kinase A and C, Raf-1, ERK, JNK, p38, c-fos, c-jun and many more[4].

Cannabis sativa preparations have been known as therapeutic agents against various diseases for millennia. The native active constituent, Delta 9-tetrahydrocannabinol (delta-9-THC) was found to be the principal mediator of the effects of cannabis[8] Δ9-THC is prescribed today under the generic name Dronabinol, to treat vomiting and for enhancement of appetite, mainly in AIDS patients.

Separation between the therapeutically undesirable psychotropic effects, and the clinically desirable ones however, has not been reported with agonists that bind to cannabinoid receptors. THC, as well as the two major endogenous compounds identified so far that bind to the cannabinoid receptors —anandamide and 2-arachidonylglycerol (2-AG)— produce most of their effects by binding to both the CB1 and CB2 cannabinoid receptors. While the effects mediated by CB1, mostly in the CNS, have been thoroughly investigated, those mediated by CB2 are not equally well defined.

ešte nejaké názorné súvislosti a bude to zrozumiteľné aj pre mňa hoci som chemik.