By Roger G. Pertwee (Editor)
The current publication is an exceptional precis of many facets of cannabinoid study. It offers present wisdom in regards to the pharmacology and healing strength of cannabinoids in addition to wisdom concerning the pharmacology, body structure, and pathology of the endogenous cannabinoid structures. The chapters are written through scientists who've made or are nonetheless making significant contributions to the sphere. This booklet might support generate novel rules on the right way to procedure the research of feelings.
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Additional resources for Cannabinoids (Handbook of Experimental Pharmacology)
Pertwee glioma cells. 7 µM in non-irradiated HL-60 cells and at 25 µM but not 10 µM in U87 and U373 glioma cells (Gallily et al. 2003; Massi et al. 2004). At these or higher concentrations, cannabidiol did not induce detectable apoptosis in γ -irradiated or non-irradiated monocytes obtained from normal individuals (Gallily et al. 2003). g. dopamine D2 and opioid receptors) (Wager-Miller et al. 2002). Resulting cross-talk between CB1 and non CB1 receptors may involve the sequestration of G proteins either from other receptor types by CB1 receptors (reviewed in Pertwee 2003) or conversely, from CB1 receptors by other receptor types.
However, the possibility does remain that it may be a novel metabotropic “vanilloid-like” receptor (see below). The proposed new receptor also differs from established cannabinoid receptors in several ways. Pharmacological Actions of Cannabinoids 29 – It is not sensitive to activation by the established CB1 /CB2 receptor agonists, ∆9 THC, CP55940 or HU-210 (Breivogel et al. 2001; Di Marzo et al. 2000; Monory et al. 2002). – It is not coupled to adenylate cyclase, at least in the cerebellum of CB1 –/– CD1 mice (Monory et al.
2001; Zygmunt et al. 1999), whereas lipoxygenase metabolites of anandamide show greater potency at these receptors than their parent compound, at least in guinea-pig bronchus (Craib et al. 2001; Pertwee and Ross 2002). The TRPV1 receptor is not activated by 2-arachidonoyl glycerol or by non-eicosanoid CB1 /CB2 receptor agonists (Zygmunt et al. 1999), although it is activated by micromolar concentrations of the phytocannabinoid cannabidiol (Bisogno et al. 2001). One compound that behaves as a potent agonist at both TRPV1 and CB1 receptors is the synthetic anandamide analogue O-1861 (Fig.
Cannabinoids (Handbook of Experimental Pharmacology) by Roger G. Pertwee (Editor)