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Genetics endocannabinoids

The endocannabinoid system might also be involved, since A9-tetrahydorcan-nabinol, the major active ingredient in cannabis, decreases somatically expressed withdrawal behaviors and the aversiveness of withdrawal in mecamylamine- and naloxone-precipitated nicotine abstinence (Balfour 2002). However, genetic knockout of the CBl cannabinoid receptors did not significantly affect somatically expressed withdrawal behaviors (Castane et al. 2002). [Pg.423]

Moreira, F. A., Kaiser, N., Monory, K., and Lutz, B. (2008). Reduced anxiety-like behaviour induced by genetic and pharmacological inhibition of the endocannabinoid-degrading enzyme fatty add amide hydrolase (FAAH) is mediated by CB1 receptors. Neuropharmacology 54, 141-150. [Pg.70]

Mitjans M, Gasto C, Catalan R et al (2012) Genetic variability in the endocannabinoid system and 12-week clinical response to cital-opram treatment the role of the CNR1, CNR2 and FAAH genes. J Psychopharmacol 26 1391-1398... [Pg.237]

Russo P, Strazzullo P, Cappuccio FP et al (2007) Genetic variations at the endocannabinoid type 1 receptor gene (CNR1) are associated with obesity phenotypes in men. J Clin Endocrinol Metab 92 2382-2386... [Pg.237]

Aberle J, Fedderwitz I, Klages N et al (2007) Genetic variation in two proteins of the endocannabinoid system and their influence on body mass index and metabolism under low fat diet. Horm Metab Res 39 395-397... [Pg.237]

The endocannabinoid system is implicated in the physiological control of food intake and energy balance, not only after food deprivation but also in animal models of genetic obesity in which it appears to become overactive at the level of both the hypothalamus and adipocytes (Di Marzo et al. 2001c Bensaid et al. 2003). This possibly explains why, following treatment of mice and rats with rimonabant, a transient inhibition of food intake and a more persistent reduction of fat mass are observed (Ravinet-Trillou et al. 2003), and why CBi knockout mice show a reduced susceptibility to obesity in response to a fat diet (Ravinet-Trillou et al. 2004). [Pg.170]

Chiang, K. P., Gerber, A. L., Sipe, J. C. and Cravatt, B. F., Reduced cellular expression and activity of the P129T mutant of human fatty acid amide hydrolase evidence for a link between defects in the endocannabinoid system and problem drug use. Hum Mol Genet, 13 (2004)2113-2119. [Pg.125]

Norrod, A. G. and Puffenbarger, R. A., Genetic polymorphisms of the endocannabinoid system, Chem Biodivers, 4 (2007) 1926-1932. [Pg.130]


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See also in sourсe #XX -- [ Pg.94 ]




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