Exposure to Far Infrared Ray Protects Methamphetamine-Induced Behavioral Sensitization in Glutathione Peroxidase-1 Knockout Mice via Attenuating Mitochondrial Burdens and Dopamine D1 Receptor Activation |
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Authors: | Huynh Nhu Mai Naveen Sharma Eun-Joo Shin Bao Trong Nguyen Ji Hoon Jeong Choon-Gon Jang Eun-Hee Cho Seung Yeol Nah Nam Hun Kim Toshitaka Nabeshima Hyoung-Chun Kim |
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Affiliation: | 1.Neuropsychopharmacology and Toxicology Program, College of Pharmacy,Kangwon National University,Chuncheon,Republic of Korea;2.Department of Pharmacology, College of Medicine,Chung-Ang University,Seoul,Republic of Korea;3.Department of Pharmacology, School of Pharmacy,Sungkyunkwan University,Suwon,Republic of Korea;4.Department of Internal Medicine, Medical School,Kangwon National University,Chuncheon,Republic of Korea;5.Ginsentology Research Laboratory and Department of Physiology, College of Veterinary Medicine,Konkuk University,Seoul,Republic of Korea;6.College of Forest and Environmental Sciences,Kangwon National University,Chuncheon,Republic of Korea;7.Advanced Diagnostic System Research Laboratory,Fujita Health University Graduate School of Health Sciences,Aichi,Japan |
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Abstract: | Evidence indicates that stress conditions might lead to drug dependence. Recently, we have demonstrated that exposure to far infrared ray (FIR) attenuates acute restraint stress via induction of glutathione peroxidase-1 (GPx-1) gene. We investigated whether FIR affects methamphetamine (MA)-induced behavioral sensitization and whether FIR-mediated pharmacological activity requires interaction between dopamine receptor and GPx-1 gene. We observed that MA treatment significantly increased GPx-1 expression in the striatum of wild-type (WT) mice. Interestingly, exposure to FIR potentiated MA-induced increase in GPx-1 expression. This phenomenon was also observed in animals receiving MA with dopamine D1 receptor antagonist SCH23390. However, dopamine D2 receptor antagonist sulpiride did not affect MA-induced GPx-1 expression. FIR exposure or SCH23390, but not sulpiride, significantly attenuated MA-induced behavioral sensitization. Exposure to FIR significantly attenuated MA-induced dopamine D1 receptor expression, c-Fos induction and oxidative burdens. FIR-mediated antioxidant effects were also more pronounced in mitochondrial- than cytosolic-fraction. In addition, FIR significantly attenuated against MA-induced changes in mitochondrial superoxide dismutase and mitochondrial GPx activities, mitochondrial transmembrane potential, intramitochondrial Ca2+ level, mitochondrial complex-I activity, and mitochondrial oxidative burdens. The attenuation by FIR was paralleled that by SCH23390. Effects of FIR or SCH23390 were more sensitive to GPx-1 KO than WT mice, while SCH23390 treatment did not exhibit any additive effects on the protective activity mediated by FIR, indicating that dopamine D1 receptor constitutes a molecular target of FIR. Our result suggests that exposure to FIR ameliorates MA-induced behavioral sensitization via possible interaction between dopamine D1 receptor and GPx-1 gene. |
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