Neuronal nicotinic acetylcholine receptors mediate ∆⁹ -THC dependence: Mouse and human studies.

ABSTRACT: Cessation from prolonged use of ∆⁹ -tetrahydrocannabinol (THC), the primary active compound responsible for the cannabimimetic effects of cannabis, results in a mild to moderate withdrawal syndrome in humans and laboratory animals. Whereas manipulations of the endogenous cannabinoid system (eg, cannabinoid receptors and endocannabinoid regulating enzymes) alter nicotine withdrawal, in this study we asked the reciprocal question. Do nicotinic acetylcholine receptors (nAChRs) modulate THC withdrawal? To assess the role of different nAChR subtypes in THC withdrawal, we used transgenic mouse, preclinical pharmacological, and human genetic correlation approaches. Our findings show that selective α3β4* nAChR antagonist, AuIB, and α3β4* nAChR partial agonist, AT-1001, dose-dependently

SUBMITTER: Donvito G 

PROVIDER: S-EPMC6509006 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature