ArticleInternational journal of molecular sciences2021
Cannabinoid Receptor Type 1 Regulates Drug Reward Behavior via Glutamate Decarboxylase 67 Transcription.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Assessment of Abuse Potential of Three Indazole-Carboxamide Synthetic Cannabinoids 5F-ADB, MDMB-4en-PINACA and ADB-4en-PINACA.International journal of molecular sciences · 2025Article
- Crystallin Alpha B Inhibits Cocaine-Induced Conditioned Place Preference via the Modulation of Dopaminergic Neurotransmission.Addiction biology · 2025Article
- Psychological, social factors, and smoking behavior mediated the effects of cannabis use on personality disorders: A Mendelian randomization study.Frontiers in psychiatry · 2025Article
- Different development patterns of reward behaviors induced by ketamine and JWH-018 in striatal GAD67 knockdown mice.Journal of veterinary science · 2024Article
- Pharmacological Treatments for Methamphetamine Use Disorder: Current Status and Future Targets.Substance abuse and rehabilitation · 2024Review
- Molecular Alterations of the Endocannabinoid System in Psychiatric Disorders.International journal of molecular sciences · 2022Review
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
Interaction of cannabinoid receptor type 1 (CB1) and GABAergic neuronal activity is involved in drug abuse-related behavior. However, its role in drug-dependent Pavlovian conditioning is not well understood. In this study, we aimed to evaluate the effects of a CB1 agonist, JWH-210, on the development of conditioned place preference (CPP)-induced by methamphetamine (METH). Pretreatment with a synthetic cannabinoid, JWH-210 (CB1 agonist), increased METH-induced CPP score and METH-induced dopamine release in acute striatal slices. Interestingly, CB1 was expressed in glutamate decarboxylase 67 (GAD67) positive cells, and overexpression of CB1 increased GAD67 expression, while CB1 knockdown reduced GAD67 expression in vivo and in vitro. GAD67 is known as an enzyme involved in the synthesis of GABA. CB1 knockdown in the mice striatum increased METH-induced CPP. When GAD67 decreased in the mice striatum, mRNA level of
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