期刊
JOURNAL OF PHARMACOLOGICAL SCIENCES
卷 136, 期 2, 页码 93-96出版社
JAPANESE PHARMACOLOGICAL SOC
DOI: 10.1016/j.jphs.2018.01.001
关键词
LPA5; Neuropathic pain; Multiple sclerosis
资金
- Ministry of Education, Culture, Sports, Science and Technology, Japan [26253077]
- Platform for Drug Discovery, Informatics, and Structural Life Science project - Japan Agency for Medical Research and Development [16am0101012j0005]
- Grants-in-Aid for Scientific Research [17K19918, 17K08287, 16K07093, 26860144, 17H01586, 26253077, 16H05136] Funding Source: KAKEN
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 A delta-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. (c) 2018 The Authors. Production and hosting by Elsevier B.V. on behalf of Japanese Pharmacological Society.
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