Attenuation Effect of Cannabinoid Type 1 Receptor Activation on Methamphetamine-Induced Neurodegeneration and Locomotion Impairments among Male Rats
Background: A number of neuroimaging studies on human addicts have revealed that abuse of Methamphetamine (METH) can induce neurodegenerative changes in various brain regions like the cerebral cortex and cerebellum. Although the underlying mechanisms of METH-induced neurotoxicity have been studied,...
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Kerman University of Medical Sciences
2017-11-01
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Series: | Addiction and Health |
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Online Access: | https://ahj.kmu.ac.ir/article_84730_4991dcec6fb5987423abb0366eb116f7.pdf |
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author | Effat Ramshini Shahriar Dabiri Shokouh Arjmand Gholamreza Sepehri Mohammad Khaksari Meysam Ahmadi Mohammad Shabani |
author_facet | Effat Ramshini Shahriar Dabiri Shokouh Arjmand Gholamreza Sepehri Mohammad Khaksari Meysam Ahmadi Mohammad Shabani |
author_sort | Effat Ramshini |
collection | DOAJ |
description | Background: A number of neuroimaging studies on human addicts have revealed that abuse of Methamphetamine (METH) can induce neurodegenerative changes in various brain regions like the cerebral cortex and cerebellum. Although the underlying mechanisms of METH-induced neurotoxicity have been studied, the cellular and molecular mechanisms of METH-induced neurotoxicity remain to be clarified. Previous studies implicated that cannabinoid type 1 receptors (CB1Rs) exert neuroprotective effects on several models of cerebral toxicity, but their role in METH-induced neurotoxicity has been rarely investigated. Moreover, the cerebellum was considered as a potential target to evaluate the effects of cannabinoids on locomotion activity as the CB1Rs are most widely distributed in the molecular layer of cerebellum. Therefore, the present study was carried out to evaluate whether neurodegeneration induced in the cerebellum tissue implicated in locomotion deficit induced by METH.Methods: In the current study, open field test was used to examine locomotor activity. Using hematoxylin and eosin (H&E) staining, morphology of the cerebellar vermis was investigated after repeated exposure to METH. Then, the effects of CB1Rs antagonist [SR17141A, 10 mg/kg, intraperitoneally (IP)] and CB1Rs agonist [WIN55, 212-2 (WIN), 3 mg/kg] against METH-induced neurodegeneration and locomotor deficit were assessed.Findings: The results of the present study demonstrated that repeated exposure to METH increased cerebellar degeneration level as compared to the saline and dimethyl sulfoxide (DMSO) groups. In addition, METH-treated rats showed hyperactivity as compared to the saline and DMSO groups. Pretreatment with WIN significantly attenuated neurodegeneration and hyperactivity induced by METH.Conclusion: The findings of this study provided evidence that CB1Rs may serve as a therapeutic strategy for attenuation of METH-induced locomotor deficits. |
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issn | 2008-4633 2008-8469 |
language | English |
last_indexed | 2024-03-11T23:51:48Z |
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publisher | Kerman University of Medical Sciences |
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series | Addiction and Health |
spelling | doaj.art-18900d2c049b4a60a8ea3d598289353b2023-09-19T06:50:18ZengKerman University of Medical SciencesAddiction and Health2008-46332008-84692017-11-019420621384730Attenuation Effect of Cannabinoid Type 1 Receptor Activation on Methamphetamine-Induced Neurodegeneration and Locomotion Impairments among Male RatsEffat Ramshini0Shahriar Dabiri1Shokouh Arjmand2Gholamreza Sepehri3Mohammad Khaksari4Meysam Ahmadi5Mohammad Shabani6PhD Candidate, Department of Physiology AND Physiology Research Center, Institute of Basic and Clinical Physiology Sciences, Kerman University of Medical Sciences, Kerman, IranProfessor, Department of Pathology, School of Medicine, Kerman University of Medical Sciences, Kerman, IranPharmacist, Intracellular Recording Lab, Neuroscience Research Center, Neuropharmacology Institute, Kerman University of Medical Sciences, Kerman, IranProfessor, Neuroscience Research Center, Neuropharmacology Institute, Kerman University of Medical Sciences, Kerman, IranProfessor, Endocrinology and Metabolism Research Center, Institute of Basic and Clinical Physiology Sciences, Kerman University of Medical Sciences, Kerman, IranAssistant Professor, Neuroscience Research Center, Neuropharmacology Institute, Kerman University of Medical Sciences, Kerman, IranAssociate Professor, Neuroscience Research Center, Neuropharmacology Institute, Kerman University of Medical Sciences, Kerman, IranBackground: A number of neuroimaging studies on human addicts have revealed that abuse of Methamphetamine (METH) can induce neurodegenerative changes in various brain regions like the cerebral cortex and cerebellum. Although the underlying mechanisms of METH-induced neurotoxicity have been studied, the cellular and molecular mechanisms of METH-induced neurotoxicity remain to be clarified. Previous studies implicated that cannabinoid type 1 receptors (CB1Rs) exert neuroprotective effects on several models of cerebral toxicity, but their role in METH-induced neurotoxicity has been rarely investigated. Moreover, the cerebellum was considered as a potential target to evaluate the effects of cannabinoids on locomotion activity as the CB1Rs are most widely distributed in the molecular layer of cerebellum. Therefore, the present study was carried out to evaluate whether neurodegeneration induced in the cerebellum tissue implicated in locomotion deficit induced by METH.Methods: In the current study, open field test was used to examine locomotor activity. Using hematoxylin and eosin (H&E) staining, morphology of the cerebellar vermis was investigated after repeated exposure to METH. Then, the effects of CB1Rs antagonist [SR17141A, 10 mg/kg, intraperitoneally (IP)] and CB1Rs agonist [WIN55, 212-2 (WIN), 3 mg/kg] against METH-induced neurodegeneration and locomotor deficit were assessed.Findings: The results of the present study demonstrated that repeated exposure to METH increased cerebellar degeneration level as compared to the saline and dimethyl sulfoxide (DMSO) groups. In addition, METH-treated rats showed hyperactivity as compared to the saline and DMSO groups. Pretreatment with WIN significantly attenuated neurodegeneration and hyperactivity induced by METH.Conclusion: The findings of this study provided evidence that CB1Rs may serve as a therapeutic strategy for attenuation of METH-induced locomotor deficits.https://ahj.kmu.ac.ir/article_84730_4991dcec6fb5987423abb0366eb116f7.pdfneurodegenerationmethamphetaminecerebellumcb1 receptor |
spellingShingle | Effat Ramshini Shahriar Dabiri Shokouh Arjmand Gholamreza Sepehri Mohammad Khaksari Meysam Ahmadi Mohammad Shabani Attenuation Effect of Cannabinoid Type 1 Receptor Activation on Methamphetamine-Induced Neurodegeneration and Locomotion Impairments among Male Rats Addiction and Health neurodegeneration methamphetamine cerebellum cb1 receptor |
title | Attenuation Effect of Cannabinoid Type 1 Receptor Activation on Methamphetamine-Induced Neurodegeneration and Locomotion Impairments among Male Rats |
title_full | Attenuation Effect of Cannabinoid Type 1 Receptor Activation on Methamphetamine-Induced Neurodegeneration and Locomotion Impairments among Male Rats |
title_fullStr | Attenuation Effect of Cannabinoid Type 1 Receptor Activation on Methamphetamine-Induced Neurodegeneration and Locomotion Impairments among Male Rats |
title_full_unstemmed | Attenuation Effect of Cannabinoid Type 1 Receptor Activation on Methamphetamine-Induced Neurodegeneration and Locomotion Impairments among Male Rats |
title_short | Attenuation Effect of Cannabinoid Type 1 Receptor Activation on Methamphetamine-Induced Neurodegeneration and Locomotion Impairments among Male Rats |
title_sort | attenuation effect of cannabinoid type 1 receptor activation on methamphetamine induced neurodegeneration and locomotion impairments among male rats |
topic | neurodegeneration methamphetamine cerebellum cb1 receptor |
url | https://ahj.kmu.ac.ir/article_84730_4991dcec6fb5987423abb0366eb116f7.pdf |
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