Cannabinoids (Handbook of Experimental Pharmacology) by Roger G. Pertwee (Editor)
By Roger G. Pertwee (Editor)
The current publication is an exceptional precis of many features of cannabinoid examine. It offers present wisdom in regards to the pharmacology and healing power of cannabinoids in addition to wisdom concerning the pharmacology, body structure, and pathology of the endogenous cannabinoid platforms. The chapters are written by way of scientists who've made or are nonetheless making significant contributions to the sphere. This ebook may perhaps aid generate novel rules on how one can technique the learn of feelings.
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Extra resources for Cannabinoids (Handbook of Experimental Pharmacology)
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).
It has also been detected in peripheral tissues. The spliced variant resembles the CB1 receptor in its afﬁnity for ∆9 -THC, CP55940 and R-(+)-WIN55212, and it also has at least two signal transduction mechanisms in common with the CB1 receptor (Rinaldi-Carmona et al. 1996a). However, the central and peripheral concentrations of CB1A mRNA are far below those of CB1 mRNA (Shire et al. 1995). Onaivi et al. (1996) have discovered three distinct CB1 mRNAs in brain tissue from C57BL/6 mice, although only one CB1 receptor cDNA.
2002). The underlying mechanism is most probably CB1 and CB2 receptor-independent, as this relaxant effect of ∆9 -THC was not prevented by 300 nM SR141716A or by 30 nM AM251 and as the CB1 /CB2 receptor agonists HU-210 and CP55940 lacked detectable relaxant activity, whereas cannabinol, which has relatively low activity as a cannabinoid receptor agonist (Sect. 1), was equipotent with ∆9 -THC. The possibility, that ∆9 -THC was acting through ionotropic or metabotropic glutamate receptors was also excluded.