LPA5 signaling is involved in multiple sclerosis-mediated neuropathic pain in the cuprizone mouse model

Ryoko Tsukahara; Shinji Yamamoto; Keisuke Yoshikawa; Mari Gotoh; Tamotsu Tsukahara; Hiroyuki Neyama; Satoshi Ishii; Noriyuki Akahoshi; Keisuke Yanagida; Hayakazu Sumida; Masatake Araki; Kimi Araki; Ken-ichi Yamamura; Kimiko Murakami-Murofushi; Hiroshi Ueda

Journal of Pharmacological Sciences (Feb 2018)

LPA5 signaling is involved in multiple sclerosis-mediated neuropathic pain in the cuprizone mouse model

Ryoko Tsukahara,
Shinji Yamamoto,
Keisuke Yoshikawa,
Mari Gotoh,
Tamotsu Tsukahara,
Hiroyuki Neyama,
Satoshi Ishii,
Noriyuki Akahoshi,
Keisuke Yanagida,
Hayakazu Sumida,
Masatake Araki,
Kimi Araki,
Ken-ichi Yamamura,
Kimiko Murakami-Murofushi,
Hiroshi Ueda

Affiliations

Ryoko Tsukahara: Department of Pharmacology and Therapeutic Innovation, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan
Shinji Yamamoto: Department of Pharmacology, Faculty of Medicine, Saitama Medical University, Saitama, Japan
Keisuke Yoshikawa: Department of Pharmacology, Faculty of Medicine, Saitama Medical University, Saitama, Japan
Mari Gotoh: Endowed Research Division of Human Welfare Sciences, Ochanomizu University, Tokyo, Japan; Institute for Human Life Innovation, Ochanomizu University, Tokyo, Japan
Tamotsu Tsukahara: Department of Pharmacology and Therapeutic Innovation, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan
Hiroyuki Neyama: Department of Pharmacology and Therapeutic Innovation, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan
Satoshi Ishii: Department of Immunology, Akita University Graduate School of Medicine, Akita, Japan
Noriyuki Akahoshi: Department of Immunology, Akita University Graduate School of Medicine, Akita, Japan
Keisuke Yanagida: Department of Biochemistry and Molecular Biology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
Hayakazu Sumida: Department of Biochemistry and Molecular Biology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
Masatake Araki: Institute of Resource Development and Analysis, Kumamoto University, Kumamoto, Japan
Kimi Araki: Institute of Resource Development and Analysis, Kumamoto University, Kumamoto, Japan
Ken-ichi Yamamura: Institute of Resource Development and Analysis, Kumamoto University, Kumamoto, Japan
Kimiko Murakami-Murofushi: Endowed Research Division of Human Welfare Sciences, Ochanomizu University, Tokyo, Japan
Hiroshi Ueda: Department of Pharmacology and Therapeutic Innovation, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan; Corresponding author. Department of Pharmacology and Therapeutic Innovation, Graduate School of Biomedical Sciences, Nagasaki University, 1-14 Bunkyo–machi, Nagasaki 852-8521, Japan. Fax: +81 95 819 2420.

Journal volume & issue: Vol. 136, no. 2
pp. 93 – 96

Abstract

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Lysophosphatidic acid (LPA) and LPA1 receptor signaling play a crucial role in the initiation of peripheral nerve injury-induced neuropathic pain through the alternation of pain-related genes/proteins expression and demyelination. However, LPA and its signaling in the brain are still poorly understood. In the present study, we revealed that the LPA5 receptor expression in corpus callosum elevated after the initiation of demyelination, and the hyperalgesia through Aδ-fibers following cuprizone-induced demyelination was mediated by LPA5 signaling. These data suggest that LPA5 signaling may play a key role in the mechanisms underlying neuropathic pain following demyelination in the brain. Keywords: LPA5, Neuropathic pain, Multiple sclerosis

Published in Journal of Pharmacological Sciences

ISSN: 1347-8613 (Print)
Publisher: Elsevier
Country of publisher: Japan
LCC subjects: Medicine: Therapeutics. Pharmacology
Website: http://www.journals.elsevier.com/journal-of-pharmacological-sciences

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