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大麻素CB1受体在甲基苯丙胺诱导的社交和识别记忆障碍中的作用。

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

作者信息

Khodamoradi Mehdi, Tirgar Fatemeh, Ghazvini Hamed, Rafaiee Raheleh, Tamijani Seyedeh Masoumeh Seyedhosseini, Karimi Narges, Yadegari Ali, Khachaki Ali Siahposht, Akhtari Javad

机构信息

Substance Abuse Prevention Research Center, Health Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran.

Department of Neuroscience, School of Advance Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran.

出版信息

Neurosci Lett. 2022 May 14;779:136634. doi: 10.1016/j.neulet.2022.136634. Epub 2022 Apr 14.

DOI:10.1016/j.neulet.2022.136634
PMID:35429587
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 (CBR) 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 CBR 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 CBR antagonist rimonabant, but not the CBR agonist WIN, prevented these negative effects of METH neurotoxicity. Thus, it seems that the CBR can be targeted to prevent the adverse effects of METH on cognition and social behavior, at least at experimental levels.

摘要

据报道,甲基苯丙胺(METH)会导致社交和识别记忆障碍。有证据表明,大麻素系统在认知加工和社交互动中具有重要的调节作用。然而,此前尚无研究调查大麻素系统在METH诱导的新物体识别(NOR)记忆缺陷和社交互动中可能发挥的作用。成年雄性大鼠接受神经毒性METH方案(每隔2小时皮下注射4次,每次6mg/kg)。一周后,在不同组中对它们进行NOR或社交互动测试。大麻素1型受体(CBR)拮抗剂利莫那班(1或3mg/kg,腹腔注射)改善了METH诱导的NOR获取、巩固和提取(但不是重新巩固)方面的损伤,以及METH诱导的社交行为损伤。给予CBR激动剂WIN 55,212-2(WIN;3或5mg/kg,腹腔注射)对METH诱导的记忆缺陷或社交行为损伤没有影响。我们的研究结果可能表明,METH神经毒性会损害社交和识别记忆。另一方面,CBR拮抗剂利莫那班而非CBR激动剂WIN可预防METH神经毒性的这些负面影响。因此,至少在实验水平上,似乎可以针对CBR来预防METH对认知和社交行为的不利影响。

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