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

Huynh Nhu Mai, Naveen Sharma, Eun Joo Shin, Bao Trong Nguyen, Phuong Tram Nguyen, Ji Hoon Jeong, Choon Gon Jang, Eun Hee Cho, Seung Yeol Nah, Nam Hun Kim, Toshitaka Nabeshima, Hyoung Chun Kim

Research output: Contribution to journalArticle

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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-ERK 1/2 , 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 ERK 1/2 phosphorylation by inhibiting PKCδ phosphorylation by bryostatin-1.

Original languageEnglish
Pages (from-to)63-76
Number of pages14
JournalNeurochemistry International
Volume116
DOIs
Publication statusPublished - 01-06-2018

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Infrared Rays
Muscarinic M1 Receptors
Methamphetamine
Protein Kinase C
Phosphorylation
Dicyclomine
Recognition (Psychology)
Nicotinic Receptors
Cholinergic Receptors
Muscarinic Receptors
Glutathione
Up-Regulation

All Science Journal Classification (ASJC) codes

  • Cellular and Molecular Neuroscience
  • Cell Biology

Cite this

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. / Exposure to far-infrared rays attenuates methamphetamine-induced recognition memory impairment via modulation of the muscarinic M1 receptor, Nrf2, and PKC. In: Neurochemistry International. 2018 ; Vol. 116. pp. 63-76.
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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-ERK 1/2 , 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 ERK 1/2 phosphorylation by inhibiting PKCδ phosphorylation by bryostatin-1.",
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Exposure to far-infrared rays attenuates methamphetamine-induced recognition memory impairment via modulation of the muscarinic M1 receptor, Nrf2, and PKC. / 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.

In: Neurochemistry International, Vol. 116, 01.06.2018, p. 63-76.

Research output: Contribution to journalArticle

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

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-ERK 1/2 , 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 ERK 1/2 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-ERK 1/2 , 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 ERK 1/2 phosphorylation by inhibiting PKCδ phosphorylation by bryostatin-1.

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