TY - JOUR
T1 - Exposure to far-infrared rays attenuates methamphetamine-induced recognition memory impairment via modulation of the muscarinic M1 receptor, Nrf2, and PKC
AU - Mai, Huynh Nhu
AU - Sharma, Naveen
AU - Shin, Eun Joo
AU - Nguyen, Bao Trong
AU - Nguyen, Phuong Tram
AU - Jeong, Ji Hoon
AU - Jang, Choon Gon
AU - Cho, Eun Hee
AU - Nah, Seung Yeol
AU - Kim, Nam Hun
AU - Nabeshima, Toshitaka
AU - Kim, Hyoung Chun
N1 - Funding Information:
This study was supported by a grant from Forestry Technology Projects (provided by the Korea Forest Service Project , No. S111415L020100 ), a grant from the Korea Food and Drug Administration ( 14182MFDS979 ), a grant from the Japan Society for the Promotion of Science (JSP , 17H04252 ), and by the Basic Science Research Program through the National Research Foundation of Korea (NRF)National Research Foundation of Korea funded by the Ministry of Science and ICT, Republic of Korea ( #NRF-2017R1A2B1003346 and #NRF-2016R1A1A1A05005201 ). Huynh Nhu Mai, Naveen Sharma, Bao Trong Nguyen, and Phuong Tram Nguyen were supported by the BK21 PLUS program. The English in this document has been checked by at least two professional editors, both native speakers of English (E-Worldediting; www.eworldeditiing.com ).
Publisher Copyright:
© 2018 Elsevier Ltd
PY - 2018/6/1
Y1 - 2018/6/1
N2 - 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, and L-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.
AB - 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, and L-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.
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U2 - 10.1016/j.neuint.2018.03.009
DO - 10.1016/j.neuint.2018.03.009
M3 - Article
C2 - 29572053
AN - SCOPUS:85044450407
SN - 0197-0186
VL - 116
SP - 63
EP - 76
JO - Neurochemistry International
JF - Neurochemistry International
ER -