ArticleAddiction & health2017
Attenuation Effect of Cannabinoid Type 1 Receptor Activation on Methamphetamine-Induced Neurodegeneration and Locomotion Impairments among Male Rats.
Article in Addiction & health, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Involvement of CB1 cannabinoid receptors in methamphetamine-related decision-making and social behavior deficits.BMC neuroscience · 2026Article
- Pharmacological Treatments for Methamphetamine Use Disorder: Current Status and Future Targets.Substance abuse and rehabilitation · 2024Review
- Comparing Cognitive Functions in Patients with Schizophrenia and Methamphetamine-Induced Psychosis with Healthy Controls.Addiction & health · 2022Article
- Occurrence of Takotsubo Cardiomyopathy after Synthetic Cannabinoid Consumption.Addiction & health · 2019Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA 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.
methodsIn 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.
findingsThe 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.
conclusionThe findings of this study provided evidence that CB1Rs may serve as a therapeutic strategy for attenuation of METH-induced locomotor deficits.
Indexed as
Identifiers
30574283PMC6294485W2801966929What OpenQuestion holds
Registered trials
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