Cannabidiol Modulating the Expression of Neurotrophin Signaling Pathways in Chronic Exposure to Methamphetamine in Rats During Abstinence Period.

IF 1 Q4 NEUROSCIENCES

Basic and Clinical Neuroscience Pub Date : 2022-09-01 DOI:10.32598/bcn.2021.3059.1

Yasaman Razavi, Mohammad Najafi, Abbas Haghparast, Fariborz Keyhanfar, Ronak Shabani, Mehdi Mehdizadeh

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Abstract

Introduction: Several neuropsychiatric disorders, such as addiction, have indicated variations in the levels of neurotrophic factors. As an extremely addictive stimulant, methamphetamine (METH) is associated with rising levels of abuse worldwide. We have recently demonstrated that repeated intracerebroventricular (ICV) of cannabidiol (CBD), the most important non-psychotomimetic compound, can lead to diminished impairing memory and hippocampal damage caused by chronic exposure to METH (CEM) in rats over the abstinence period. Furthermore, the results indicated a possible contribution of the neurotrophin signaling pathway (NSP) in regulating neurogenesis and survival. This study intends to evaluate whether these effects remained as measured in molecular pathways after the abstinence period.

Methods: The animals were given 2mg/kg METH twice a day for 10 days. Then, we adopted real-time polymerase chain reaction (PCR) throughout the 10-day abstinence period to assess the CBD's effect (10 and 50μg/5μL) on the levels of the mRNA expression of the NSP.

Results: The findings suggested that CEM, when compared to the control group in the hippocampus, downregulated mRNA expression of NSP. Moreover, a dosage of 50 μg/5μL CBD may possibly enhance the mRNA expression level of BDNF/TrkB and NGF/TrkA in the hippocampus. Besides, the expression of RAF-1 mRNA level could be reversed significantly by both doses of CBD.

Conclusion: According to our results, CBD may partly bring about neuroprotective effects by modulating the NSP. These findings set forth solid evidence demonstrating that CBD is a protective factor attributed to neuropsychiatric disorders, such as METH addiction.

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大麻二酚在大鼠禁欲期长期暴露于甲基苯丙胺中调节神经营养素信号通路的表达。

引言：一些神经精神疾病，如成瘾，表明神经营养因子水平存在差异。甲基苯丙胺作为一种极易成瘾的兴奋剂，与全球滥用水平的上升有关。我们最近已经证明，大麻二酚（CBD）是最重要的非拟精神病化合物，在侧脑室内重复（ICV）可以减少大鼠在禁欲期内长期暴露于甲基安非他明（CEM）引起的记忆损伤和海马损伤。此外，研究结果表明，神经营养因子信号通路（NSP）可能在调节神经发生和存活方面发挥作用。本研究旨在评估禁欲期后，这些影响是否仍如分子途径所测量的那样。方法：每天2次，每次2mg/kg，连续10天。然后，我们在整个10天的禁欲期内采用实时聚合酶链式反应（PCR）来评估CBD（10和50μg/5μL）对NSP mRNA表达水平的影响。结果：与对照组相比，CEM在海马中下调了NSP的mRNA表达。此外，50μg/5μL CBD剂量可能提高海马BDNF/TrkB和NGF/TrkA的mRNA表达水平。此外，两种剂量的CBD都可以显著逆转RAF-1 mRNA的表达。结论：CBD可能通过调节NSP而产生部分神经保护作用。这些发现提供了确凿的证据，证明CBD是神经精神障碍（如METH成瘾）的保护因素。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Basic and Clinical Neuroscience NEUROSCIENCES-

CiteScore

2.60

自引率

0.00%

发文量

审稿时长

4 weeks

期刊介绍： BCN is an international multidisciplinary journal that publishes editorials, original full-length research articles, short communications, reviews, methodological papers, commentaries, perspectives and “news and reports” in the broad fields of developmental, molecular, cellular, system, computational, behavioral, cognitive, and clinical neuroscience. No area in the neural related sciences is excluded from consideration, although priority is given to studies that provide applied insights into the functioning of the nervous system. BCN aims to advance our understanding of organization and function of the nervous system in health and disease, thereby improving the diagnosis and treatment of neural-related disorders. Manuscripts submitted to BCN should describe novel results generated by experiments that were guided by clearly defined aims or hypotheses. BCN aims to provide serious ties in interdisciplinary communication, accessibility to a broad readership inside Iran and the region and also in all other international academic sites, effective peer review process, and independence from all possible non-scientific interests. BCN also tries to empower national, regional and international collaborative networks in the field of neuroscience in Iran, Middle East, Central Asia and North Africa and to be the voice of the Iranian and regional neuroscience community in the world of neuroscientists. In this way, the journal encourages submission of editorials, review papers, commentaries, methodological notes and perspectives that address this scope.