2022
Khodamoradi, Mehdi; Tirgar, Fatemeh; Ghazvini, Hamed; Rafaiee, Raheleh; Tamijani, Seyedeh Masoumeh Seyedhosseini; Karimi, Narges; Yadegari, Ali; Khachaki, Ali Siahposht; Akhtari, Javad
Role of the cannabinoid CB1 receptor in methamphetamine-induced social and recognition memory impairment Journal Article
In: Neuroscience Letters, vol. 779, pp. 136634, 2022, ISSN: 1872-7972.
Abstract | Links | BibTeX | Tags: 212–2, Animals, Cannabinoid, Cannabinoid CB1 receptor, Cannabinoid Receptor Antagonists, Cannabinoids, CB1, Male, Memory Disorders, Methamphetamine, Neurotoxicity Syndromes, Novel object recognition memory, Rats, Receptor, Rimonabant, Social interaction, WIN 55
@article{khodamoradi_role_2022,
title = {Role of the cannabinoid CB1 receptor in methamphetamine-induced social and recognition memory impairment},
author = {Mehdi Khodamoradi and Fatemeh Tirgar and Hamed Ghazvini and Raheleh Rafaiee and Seyedeh Masoumeh Seyedhosseini Tamijani and Narges Karimi and Ali Yadegari and Ali Siahposht Khachaki and Javad Akhtari},
doi = {10.1016/j.neulet.2022.136634},
issn = {1872-7972},
year = {2022},
date = {2022-05-01},
journal = {Neuroscience Letters},
volume = {779},
pages = {136634},
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.},
keywords = {212–2, Animals, Cannabinoid, Cannabinoid CB1 receptor, Cannabinoid Receptor Antagonists, Cannabinoids, CB1, Male, Memory Disorders, Methamphetamine, Neurotoxicity Syndromes, Novel object recognition memory, Rats, Receptor, Rimonabant, Social interaction, WIN 55},
pubstate = {published},
tppubtype = {article}
}
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.