Quetiapine-induced Place Preference in Mice: Possible Dopaminergic Pathway
Autor: | Yusuf S. Althobaiti |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
medicine.drug_class medicine.medical_treatment Pharmaceutical Science Atypical antipsychotic lcsh:Medicine lcsh:RS1-441 Pharmacology Article lcsh:Pharmacy and materia medica 03 medical and health sciences 0302 clinical medicine Dopamine receptor D1 Management of schizophrenia Drug Discovery Medicine Saline reward business.industry Dopaminergic lcsh:R Antagonist quetiapine conditioned place preference Conditioned place preference abuse 030104 developmental biology Molecular Medicine Quetiapine business 030217 neurology & neurosurgery medicine.drug |
Zdroj: | Pharmaceuticals, Vol 14, Iss 156, p 156 (2021) Pharmaceuticals Volume 14 Issue 2 |
ISSN: | 1424-8247 |
Popis: | Quetiapine, an atypical antipsychotic, is effective in the management of schizophrenia, depression, and anxiety. Although quetiapine overdosage and misuse have been reported, its abuse potential has not been investigated in animals. In this study, the abuse potential of quetiapine was assessed based on the conditioned place preference (CPP) paradigm of drug addiction in a mouse model. First, mice received intraperitoneal injections of quetiapine (40, 80, or 120 mg/kg) every other day during the conditioning phase. In the second experiment, mice were pretreated with 0.03 mg/kg SKF-35866, a D1 receptor antagonist, before receiving saline or quetiapine (120 mg/kg) during the conditioning phase. No significant changes in time spent in the quetiapine-paired chamber were observed compared with time spent in the saline-paired chamber in mice treated with 40 or 80 mg/kg. In contrast, the preference to the quetiapine-paired chamber was significantly increased in mice treated with 120 mg/kg quetiapine, and this effect was blocked by SKF-35866 pretreatment. These results demonstrated, for the first time, the abuse potential of quetiapine in an animal model of drug addiction. Interestingly, this CPP-inducing effect was likely mediated by activating D1 receptors. |
Databáze: | OpenAIRE |
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