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Role of the Cannabinoid Cb1 Receptor in Methamphetamine-Induced Social and Recognition Memory Impairment Publisher Pubmed



Khodamoradi M1 ; Tirgar F2 ; Ghazvini H3, 4 ; Rafaiee R4 ; Tamijani SMS4 ; Karimi N5 ; Yadegari A3 ; Khachaki AS3 ; Akhtari J6
Authors
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Authors Affiliations
  1. 1. Substance Abuse Prevention Research Center, Health Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran
  2. 2. Department of Neuroscience, School of Advance Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran
  3. 3. Psychiatry and Behavioral Sciences Research Center, Addiction Institute, Mazandaran University of Medical Sciences, Sari, Iran
  4. 4. Department of Neuroscience, School of Advanced Technologies in Medicine, Mazandaran University of Medical Sciences, Sari, Iran
  5. 5. Department of Neurology, Clinical Research Development Unit of Bou Ali Sina Hospital, Mazandaran University of Medical Sciences, Sari, Iran
  6. 6. Department of Medical Nanotechnology, School of Advanced Technologies in Medicine, Mazandaran University of Medical Sciences, Sari, Iran

Source: Neuroscience Letters Published:2022


Abstract

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 (CB1R) 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 CB1R 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 CB1R antagonist rimonabant, but not the CB1R agonist WIN, prevented these negative effects of METH neurotoxicity. Thus, it seems that the CB1R can be targeted to prevent the adverse effects of METH on cognition and social behavior, at least at experimental levels. © 2022
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