Effects of the cannabinoid CB1 receptor antagonist, SR141716A, after Δ9-tetrahydrocannabinol withdrawal
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Delta-9-tetrahydrocannabinol
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Cannabinoid receptor antagonist
Abstract Repeated administration (5 mg kg−1 day−1 i.v.) of Δ8-tetrahydrocannabinol and its active metabolite, 11-hydroxy-Δ8-tetrahydrocannabinol caused tolerance to develop to their prolonging effect on pentobarbitone-induced sleep in mice. Reciprocal cross-tolerance also developed after seven daily doses of these cannabinoids. The magnitude of the tolerance developed by the metabolite was greater than that by Δ8-tetrahydrocannabinol. The results suggest that 11-hydroxy-Δ8-tetrahydrocannabinol plays an important role both in the sleep-prolonging effect of Δ8-tetrahydrocannabinol and its tolerance development.
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A microsuspension of Delta(9)-tetrahydrocannabinol and of its metabolic derivative 11-OH-Delta(9)-tetrahydrocannabinol has been prepared with 25 percent human serum albumin as the vehicle. Intravenous infusion of this preparation to humans indicates that both tetrahydrocannabinols are equally potent in producing the typical marihuana-like pschological and physiological effects.
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Delta-9-Tetrahydrocannabinol (0.31 mg - 1.25 mg per kg body weight) given to immunized rats by intraperitoneal injection depresses the activity of macrophage migration inhibition factor. The lowest levels of activity in peritoneal exudates were observed 15 hours after the injection of cannabinoid. This decreased activity may be related to the impaired cellular immunity observed in regular users of cannabis.
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Delta-9-tetrahydrocannabinol
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Rimonabant
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This chapter discusses the pharmacology of delta-9-tetrahydrocannabinol (THC). Topics covered include the isolation of THC from cannabis, man-made cannabinoids, cannabinoid antagonists, elimination of THC from the body, how THC works, and physiological effects of THC.
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Delta-9-tetrahydrocannabinol
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Δ9-tetrahydrocannabinol
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Repeated voluntary consumption of cannabis in milk (approximately 8 mg per day for 15 days) produced in mice tolerance to the hypothermic effect of tritiated Delta(1)-tetrahydrocannabinol ([(3)H]-Delta(1)-THC; 2 mg/kg i.v.) but not to the effect of [(3)H]-Delta(1)-THC on immobility index. The development of tolerance was not accompanied by any detectable change in levels of radioactivity in the brain assigned to Delta(1)-THC or its metabolites. It was concluded that changes in metabolism or distribution of Delta(1)-THC are not responsible for tolerance at least to the hypothermic effect of Delta(1)-THC in mice.
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