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The present paper synthetically reviews the multiple experimental lines of evidence indicating the ability of the prototypic cannabinoid CB(1) receptor antagonist, rimonabant (also known as SR 141716), to suppress the reinforcing/rewarding properties of different drugs of abuse, including cocaine, heroin, nicotine and alcohol, in laboratory rodents. This paper also reviews the data demonstrating that rimonabant reduces food intake and body weight in laboratory animals and humans. Taken together, the data reviewed here suggest that rimonabant may constitute a new and potentially effective medication for the treatment of drug addiction and obesity-related disorders.

By using Gas Chromatography-Mass Spectrometry high concentrations of endogenous gamma-hydroxybutyric acid (GHB) have been demonstrated in the rat and mouse gastrointestinal tract, including stomach, small intestine and colon-rectum. GHB concentrations were many folds higher than those present in the brain. High GHB concentrations have been also found in the human operatory specimen of sigmoid colon. Since GHB administration has been found to modify gastrointestinal motility via GABA(B) receptors, the present results suggest that endogenous GHB might be involved in the GABA(B) receptor-mediated control of gastrointestinal function.

The effect of acutely administered gamma-hydroxybutyric acid (GHB) and GHB receptor antagonist, NCS-382, on the propulsive activity in the mouse small intestine was assessed by measuring the transit of an orally administered, non absorbable marker. Both GHB (0, 25, 50, 100, 200 and 300 mg/kg; i.p.) and NCS-382 (0, 25, 50 and 75 mg/kg; i.p.) induced a dose-dependent inhibition (up to 50–60%) of the marker transit. Pretreatment with the GABA B receptor antagonist, SCH 50911 (100 mg/kg; i.p.), resulted in the blockade of the inhibiting effect of both GHB and NCS-382. These results suggest that the constipating effect of GHB and NCS-382 are secondary to stimulation of the GABA B receptor.