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

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

doi:10.32598/bcn.2021.3059.1

Volume 13, Issue 5 (September & October 2022) BCN 2022, 13(5): 719-730 | Back to browse issues page

‎ 10.32598/bcn.2021.3059.1

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Razavi Y, Najafi M, Haghparast A, Keyhanfar F, Shabani R, Mehdizadeh M. Cannabidiol Modulating the Expression of Neurotrophin Signaling Pathways in Chronic Exposure to Methamphetamine in Rats During Abstinence Period. BCN 2022; 13 (5) :719-730
URL: http://bcn.iums.ac.ir/article-1-2009-en.html

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

Yasaman Razavi¹

, Mohammad Najafi²

, Abbas Haghparast³

, Fariborz Keyhanfar⁴

, Ronak Shabani⁵

, Mehdi Mehdizadeh ^*

⁵

1- Cellular and Molecular Research Center, Iran University of Medical Sciences, Tehran, Iran.
2- Department of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
3- Neuroscience Research Center, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
4- Department of Pharmacology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
5- Reproductive Sciences and Technology Research Center, Department of Anatomy, Iran University of Medical Sciences, Tehran, Iran.

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.

Keywords: Methamphetamine, Cannabidiol, Neurotrophin signaling pathway, Chronic exposure, Abstinence, Hippocampus

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Type of Study: Original | Subject: Behavioral Neuroscience
Received: 2020/11/28 | Accepted: 2021/01/9 | Published: 2022/09/11

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