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J Pharmacol Sci. 2018 Feb;136(2):93-96. doi: 10.1016/j.jphs.2018.01.001. Epub 2018 Feb 2.

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

Author information

1
Department of Pharmacology and Therapeutic Innovation, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
2
Department of Pharmacology, Faculty of Medicine, Saitama Medical University, Saitama, Japan.
3
Endowed Research Division of Human Welfare Sciences, Ochanomizu University, Tokyo, Japan; Institute for Human Life Innovation, Ochanomizu University, Tokyo, Japan.
4
Department of Immunology, Akita University Graduate School of Medicine, Akita, Japan.
5
Department of Biochemistry and Molecular Biology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
6
Institute of Resource Development and Analysis, Kumamoto University, Kumamoto, Japan.
7
Endowed Research Division of Human Welfare Sciences, Ochanomizu University, Tokyo, Japan.
8
Department of Pharmacology and Therapeutic Innovation, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan. Electronic address: ueda@nagasaki-u.ac.jp.

Abstract

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; Multiple sclerosis; Neuropathic pain

PMID:
29409686
DOI:
10.1016/j.jphs.2018.01.001
[Indexed for MEDLINE]
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