By Pertwee, Roger G.; Abood, Mary Ellen
Lower than two decades in the past the ?eld of hashish and the cannabinoids was once nonetheless c- sidered a minor, a bit of old fashioned, quarter of analysis. a couple of teams have been energetic within the ?eld, however it was once already being considered as stagnating. The chemistry of hashish nine nine used to be renowned, ? -tetrahydrocannabinol (? -THC), identi?ed in 1964, being the single significant psychoactive constituent and cannabidiol, which isn't psychoactive, in all probability contributing to a couple of the consequences. those cannabinoids and a number of other s- thetic analogs were completely investigated for his or her pharmacological results. Their mode of motion used to be thought of to be non-speci?c. the explanations for this - sumption have been either technical and conceptual. at the technical part, it have been proven that THC was once lively in either enantiomeric varieties (though with a distinct point of efficiency) and this commentary used to be incompatible with motion on organic substrates―a receptor, an enzyme, an ion channel―which react with a unmarried stereoisomer purely. The conceptual challenge regarding THC task. This were mentioned via a number of very hot study teams that had proven that the various results visible with cannabinoids have been relating to these of biologically lively lipophiles, and that a number of the results of THC, fairly power ones, have been resembling these visible with anaesthetics and solvents
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2003) also obtained evidence that the production of 2-arachidonoyl glycerol by microglial cells can be increased by a pathological stimulus, it may be that a CB2 receptor antagonist and/or an antagonist of the putative abnormal-cannabidiol receptor could come to play a part in the clinical management of neuroinﬂammation. More recently, evidence has emerged that BV-2 microglial cells express non-CB1 , non-CB2 , non-CB2 -like, non-TRPV1, non-abnormal-cannabidiol Gi /Go -coupled-receptors upon which the endogenous fatty acid amide palmitoylethanolamide can act at concentrations in the low nanomolar range to potentiate anandamide- but not 2-arachidonoyl glycerol-induced migration of these cells (Franklin et al.
This could explain why the CB1 -selective agonist ACPA (Sect. 1), induces microglial cell migration at concentrations well below those at which it has been reported to bind to CB2 receptors, as this compound appears to induce migration by acting on both abnormal-cannabidiol-sensitive receptors and CB2 receptors (Franklin and Stella 2003). By itself, cannabidiol behaves as a weak partial agonist, producing a slight enhancement of basal migration (EC50 =250 nM) (Walter et al. 2003). Microglial cells are thought to migrate towards Pharmacological Actions of Cannabinoids 35 neuroinﬂammatory lesion sites and to release proinﬂammatory cytokines and cytotoxic agents at these sites.
J Pharmacol Exp Ther 273:1172–1181 Ahluwalia J, Yaqoob M, Urban L, Bevan S, Nagy I (2003) Activation of capsaicin-sensitive primary sensory neurones induces anandamide production and release. J Neurochem 84:585–591 Akinshola BE, Chakrabarti A, Onaivi ES (1999a) In-vitro and in-vivo action of cannabinoids. Neurochem Res 24:1233–1240 Akinshola BE, Taylor RE, Ogunseitan AB, Onaivi ES (1999b) Anandamide inhibition of recombinant AMPA receptor subunits in Xenopus oocytes is increased by forskolin and 8-bromo-cyclic AMP.
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