Cannabinoids by Pertwee, Roger G.; Abood, Mary Ellen

By Pertwee, Roger G.; Abood, Mary Ellen

Under two decades in the past the ?eld of hashish and the cannabinoids used to be nonetheless c- sidered a minor, a bit old fashioned, sector of study. a number of teams have been energetic within the ?eld, however it used to be 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 likelihood contributing to a couple of the results. those cannabinoids and several other s- thetic analogs were completely investigated for his or her pharmacological results. Their mode of motion was once thought of to be non-speci?c. the explanations for this - sumption have been either technical and conceptual. at the technical part, it were proven that THC used to be lively in either enantiomeric varieties (though with a unique point of efficiency) and this commentary was once incompatible with motion on organic substrates―a receptor, an enzyme, an ion channel―which react with a unmarried stereoisomer purely. The conceptual challenge with regards to THC job. This were mentioned by way of a number of very hot examine teams that had proven that a number of the results noticeable with cannabinoids have been regarding these of biologically lively lipophiles, and that some of the results of THC, relatively persistent ones, have been equivalent to these noticeable with anaesthetics and solvents

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They have been found to displace [3 H]SR141716A from binding sites on mouse cerebellar membranes with respectively three and eight times less potency than SR141716A (Gatley et al. 1998), and both compounds have also been shown to bind more readily to CB1 than CB2 receptors (Table 3). g. Cosenza et al. 2000; Gifford et al. 1997; Hájos and Freund 2002a; Lan et al. 1999a; Simoneau et al. 2001). Although SR141716A is CB1 -selective, it is not CB1 -specific. Thus, results from binding experiments indicate that whilst it may be reasonable to assume that concentrations of this ligand in the low or mid nanomolar range will interact mainly with the CB1 receptors when it is applied to tissues that contain both CB1 and CB2 receptors, this is not so for higher concentrations of SR141716A (Table 3).

E. that palmitoylethanolamide acts through CB1 or TRPV1 receptors, can be ruled out. Thus, it produces antinociceptive effects that are not opposed by SR141716A (Calignano et al. 1998, 2001; Farquhar-Smith et al. 2002; Farquhar-Smith and Rice 2001) and it has been found not to attenuate nociceptive behaviour induced in mice by intraplantar injection of capsaicin (Calignano et al. 2001). Also, palmitoylethanolamide does not bind to or activate CB1 receptors at concentrations below 1 or 10 µM (Devane et al.

SR141716A and SR144528 do not appear to be competitive antagonists for this putative receptor (Breivogel et al. 2001; Monory et al. 2002). – There are no specific binding sites for [3 H]CP55940 on CB1 –/– C57BL/6 mouse brain membranes (Breivogel et al. 2001). It has also been found that [3 H]R-(+)-WIN55212 undergoes selective binding to CB1 –/– C57BL/6 membranes obtained from brain areas in which R-(+)-WIN55212 enhances [35 S]GTPγ S binding (cerebral cortex, hippocampus and brain stem) (Breivogel et al.

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