Role of the cannabinoid CB1 receptor in methamphetamine-induced social and recognition memory impairment.

• METH regimen impaired social interaction and the acquisition, consolidation, retrieval, and reconsolidation of NOR. • Rimonabant improved METH-induced deficits of the acquisition, consolidation, and retrieval, but not reconsolidation, of NOR. • Rimonabant improved METH-induced impairment of social behavior. • WIN administration did not affect deficits in memory and social behavior induced by METH. Methamphetamine (METH) has been reported to induce social and recognition memory impairment. Evidence suggests that the cannabinoid system has an important modulatory role in cognitive processing and social interaction. Nonetheless, no previous study has investigated the probable role of the cannabinoids system on METH-induced deficits of novel object recognition (NOR) memory and social interaction. Adult male rats were given a neurotoxic METH regimen (four injections of 6 mg/kg, s.c, at 2 h intervals). One week later, they were examined for either NOR or social interaction in different groups. The cannabinoid type 1 receptor (CB 1 R) antagonist rimonabant (1 or 3 mg/kg, i.p.) improved METH-induced impairment of the acquisition, consolidation, and retrieval, but not reconsolidation, of NOR and also METH-induced impairment of social behavior. Administration of the CB 1 R agonist WIN 55,212–2 (WIN; 3 or 5 mg/kg, i.p.) did not affect memory deficits or social behavior impairment induced by METH. Our findings may indicate that METH neurotoxicity impairs social and recognition memory. On the other hand, the CB 1 R antagonist rimonabant, but not the CB 1 R agonist WIN, prevented these negative effects of METH neurotoxicity. Thus, it seems that the CB 1 R can be targeted to prevent the adverse effects of METH on cognition and social behavior, at least at experimental levels. [ABSTRACT FROM AUTHOR]