Tsukahara Ryoko, Yamamoto Shinji, Yoshikawa Keisuke, Gotoh Mari, Tsukahara Tamotsu, Neyama Hiroyuki, Ishii Satoshi, Akahoshi Noriyuki, Yanagida Keisuke, Sumida Hayakazu, Araki Masatake, Araki Kimi, Yamamura Ken-Ichi, Murakami-Murofushi Kimiko, Ueda Hiroshi
Department of Pharmacology and Therapeutic Innovation, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Department of Pharmacology, Faculty of Medicine, Saitama Medical University, Saitama, Japan.
J Pharmacol Sci. 2018 Feb;136(2):93-96. doi: 10.1016/j.jphs.2018.01.001. Epub 2018 Feb 2.
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.
溶血磷脂酸（LPA）和LPA1受体信号传导通过改变疼痛相关基因/蛋白质表达和脱髓鞘在周围神经损伤诱导的神经性疼痛的起始中起关键作用。然而，LPA及其在大脑中的信号传导仍知之甚少。在本研究中，我们发现胼胝体中的LPA5受体表达在脱髓鞘开始后升高，并且铜离子螯合剂诱导脱髓鞘后通过Aδ纤维的痛觉过敏由LPA5信号传导介导。这些数据表明，LPA5信号传导可能在脑脱髓鞘后神经性疼痛的潜在机制中起关键作用。
