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

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

研究成果: Article

8 引用 (Scopus)

抄録

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.

元の言語English
ページ(範囲)1294-1310
ページ数17
ジャーナルJournal of Neuroscience Research
96
発行部数7
DOI
出版物ステータスPublished - 01-07-2018

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Infrared Rays
Methamphetamine
Clozapine
Protein Kinase C
Antipsychotic Agents
Mitogen-Activated Protein Kinase 3
Mitogen-Activated Protein Kinase 1
Glutathione
NF-E2-Related Factor 2
Genes
Recognition (Psychology)
Inhibition (Psychology)
Prefrontal Cortex
Isoenzymes
Up-Regulation
Down-Regulation
Antioxidants
Phosphorylation

All Science Journal Classification (ASJC) codes

  • Cellular and Molecular Neuroscience

これを引用

Mai, Huynh Nhu ; Sharma, Naveen ; Shin, Eun Joo ; Nguyen, Bao Trong ; Nguyen, Phuong Tram ; Jeong, Ji Hoon ; Cho, Eun Hee ; Lee, Yu Jeung ; Kim, Nam Hun ; Jang, Choon Gon ; Nabeshima, Toshitaka ; Kim, Hyoung Chun. / 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. :: Journal of Neuroscience Research. 2018 ; 巻 96, 番号 7. pp. 1294-1310.
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abstract = "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.",
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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. / Mai, Huynh Nhu; Sharma, Naveen; Shin, Eun Joo; Nguyen, Bao Trong; Nguyen, Phuong Tram; Jeong, Ji Hoon; Cho, Eun Hee; Lee, Yu Jeung; Kim, Nam Hun; Jang, Choon Gon; Nabeshima, Toshitaka; Kim, Hyoung Chun.

:: Journal of Neuroscience Research, 巻 96, 番号 7, 01.07.2018, p. 1294-1310.

研究成果: Article

TY - JOUR

T1 - Exposure to far-infrared ray attenuates methamphetamine-induced impairment in recognition memory through inhibition of protein kinase C δ in male mice

T2 - Comparison with the antipsychotic clozapine

AU - Mai, Huynh Nhu

AU - Sharma, Naveen

AU - Shin, Eun Joo

AU - Nguyen, Bao Trong

AU - Nguyen, Phuong Tram

AU - Jeong, Ji Hoon

AU - Cho, Eun Hee

AU - Lee, Yu Jeung

AU - Kim, Nam Hun

AU - Jang, Choon Gon

AU - Nabeshima, Toshitaka

AU - Kim, Hyoung Chun

PY - 2018/7/1

Y1 - 2018/7/1

N2 - 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.

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