Exposure to far-infrared rays attenuates methamphetamine-induced recognition memory impairment via modulation of the muscarinic M1 receptor, Nrf2, and PKC. (June 2018)

• Record Type: Journal Article
• Authors: Mai, Huynh Nhu; Sharma, Naveen; Shin, Eun-Joo; Nguyen, Bao Trong; Nguyen, Phuong Tram; Jeong, Ji Hoon; Jang, Choon-Gon; Cho, Eun-Hee; Nah, Seung-Yeol; Kim, Nam Hun; Nabeshima, Toshitaka; Kim, Hyoung-Chun
• Is Part Of: Neurochemistry international. Volume 116(2018)
• Page Start: 63
• Page End: 76
• Publication Date: 2018-06
• Subjects: Far-infrared rays -- Methamphetamine-induced memory impairment -- Protein kinase C activation -- Glutathione system -- M1 muscarinic acetylcholine receptor -- Prefrontal cortex; Neurochemistry -- Periodicals; Neurochemistry -- Periodicals; Neurochimie -- Périodiques; Neurochemistry; Periodicals; 612.804205
• DOI: 10.1016/j.neuint.2018.03.009
• Languages: English
• ISSNs: 0197-0186

Abstract

Abstract: We demonstrated that activation of protein kinase Cδ (PKCδ) and inactivation of the glutathione peroxidase-1 (GPx-1)-dependent systems are critical for methamphetamine (MA)-induced recognition memory impairment. We also demonstrated that exposure to far-infrared rays (FIR) causes induction of the glutathione (GSH)-dependent system, including induction of the GPx-1 gene. Here, we investigated whether exposure to FIR rays affects MA-induced recognition memory impairment and whether it modulates PKC, cholinergic receptors, and the GSH-dependent system. Because the PKC activator bryostatin-1 mainly induces PKCα, PKCε, and PKCδ, we assessed expression of these proteins after MA treatment. MA treatment selectively increased PKCδ expression and its phosphorylation. Exposure to FIR rays significantly attenuated MA-induced increases in PKCδ phosphorylation. Importantly, bryostatin-1 potentiated MA-induced phosphorylation of PKCδ. MA treatment significantly decreased M1, M3, and M4 muscarinic acetylcholine receptors (mAChRs) and β2 nicotinic acetylcholine receptor expression. Of these, the decrease was most pronounced in M1 mAChR. Exposure to FIR significantly attenuated MA-induced decreases in the M1 mAChR and phospho-ERK1/2, while it facilitated Nrf2-dependent GSH induction. Dicyclomine, an M1 mAChR antagonist, andl -buthionine-(S, R)-sulfoximine (BSO), an inhibitor of GSH synthesis, counteracted against the protective potentials mediated by FIR. More importantly, the memory-enhancing potential of FIR rays was significantly counteracted by bryostatin-1, dicyclomine, and BSO. Our results suggest that exposure to FIR rays attenuates MA-induced impairment in recognition memory via up-regulation of M1 mAChR, Nrf2-dependent GSH induction, and ERK1/2 phosphorylation by inhibiting PKCδ phosphorylation by bryostatin-1. Highlights: FIR attenuated MA-induced memory dysfunction via inhibition of PKCδ phosphorylation. FIR potentiated MA-induced compensative induction in Nrf2 and GCLs levels. Inhibition of PKCδ phosphorylation activated M1 mAChR/Nrf-2/ERK1/2 signaling. Protective activity of FIR was counteracted by PKC activation, dicyclomine, and BSO.