Pain research continues to be controversial, partly because the public does not realize opiates generally don’t help central pain (except by sedation); but also because the receptors which produce pain in the cell membrane are responsive to a variety of drugs, some of them illegal, (such as opioids and cannabioids)
This article is by no means to be construed as advocating long term use of cannabinoids. This behavior has already been shown to predispose to lung cancer. However, the truth must be told. It would appear that activation of the cannabinoid 1 receptor in the brain DOES have a neuroprotective effect. Although these studis are begin funded by those interested in preventing aging, as stepchildren of medicine, we will be glad to borrow the information for what it tells us about pain.
Kim et al writing in Mol Pharmacol. 2006 Mar;69(3):691-6 have shown that the Cannabinoid 1 receptor activation protects against NMDA toxicity*, most probably by inhibiting production of nitric oxide (NO) and protein kinase A, a known pain exciter. (see PKA and NO info using SEARCH at this site for more information on how these chemicals act as pain exciters).
Greenberg and his colleagues such as Kim at the Buck Instititute in Novato California are not unsupported in this conclusion.
Martini, et al at UCSF (See FASEB J, 2006 Dec 28 showed that Ligand-induced down-regulation of the Cannabinoid ! receptor is mediated by the G-protein coupled receptor-associated sorting protein. How a G protein works is explained at this site in detail–use SEARCH if you are curious.
As Martini points out,
