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J Neurosci Res. 2018 Jul;96(7):1294-1310. doi: 10.1002/jnr.24228. Epub 2018 Feb 24.

Exposure to far-infrared ray attenuates methamphetamine-induced impairment in recognition memory through inhibition of protein kinase C δ in male mice: Comparison with the antipsychotic clozapine.

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Neuropsychopharmacology and Toxicology Program, College of Pharmacy, Kangwon National University, Chunchon, Republic of Korea.
Department of Pharmacology, College of Medicine, Chung-Ang University, Seoul, Republic of Korea.
Department of Internal Medicine, Medical School, Kangwon National University, Chunchon, Republic of Korea.
Clinical Pharmacology, College of Pharmacy, Kangwon National University, Chunchon, Republic of Korea.
College of Forest and Environmental Sciences, Kangwon National University, Chunchon, Republic of Korea.
Department of Pharmacology, School of Pharmacy, Sungkyunkwan University Suwon, Korea.
Advanced Diagnostic System Research Laboratory, Fujita Health University Graduate School of Health Sciences, Aichi, Japan.
Aino University, Ibaragi, Japan.


We have previously demonstrated that repeated treatment with methamphetamine (MA) results in a recognition memory impairment via upregulation of protein kinase C (PKC) δ and downregulation of the glutathione peroxidase-1 (GPx-1)-dependent antioxidant system. We also demonstrated that far-infrared ray (FIR) attenuates acute restraint stress via induction of the GPx-1 gene. Herein, we investigated whether exposure to FIR modulates MA-induced recognition memory impairment in male mice, and whether cognitive potentials mediated by FIR require modulation of the PKCδ gene, extracellular signal-regulated kinase (ERK) 1/2, and glutathione-dependent system. Repeated treatment with MA significantly increased PKCδ expression and its phosphorylation out of PKC isoenzymes (i.e., PKCα, PKCβI, PKCβII, PKCζ, and PKCδ expression) in the prefrontal cortex of mice. Exposure to FIR significantly attenuated MA-induced increase in phospho-PKCδ and decrease in phospho-ERK 1/2. In addition, FIR further facilitated the nuclear factor E2-related factor 2 (Nrf2)-dependent glutathione synthetic system. Moreover, L-buthionine-(S, R)-sulfoximine, an inhibitor of glutathione synthesis, counteracted the FIR-mediated phospho-ERK 1/2 induction and memory-enhancing activity against MA insult. More important, positive effects of FIR are comparable to those of genetic depletion of PKCδ or the antipsychotic clozapine. Our results indicate that FIR protects against MA-induced memory impairment via activations of the Nrf2-dependent glutathione synthetic system, and ERK 1/2 signaling by inhibition of the PKCδ gene.


extracellular signal-regulated kinase 1/2; far-infrared rays; glutathione system; methamphetamine-induced memory impairment; protein kinase C δ knockout mice


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