LPA5 signaling is involved in multiple sclerosis-mediated neuropathic pain in the cuprizone mouse model
LPA5 signaling is involved in multiple sclerosis-mediated neuropathic pain in the cuprizone mouse model
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DOI：
10.1016/j.jphs.2018.01.001
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发表时间：
2018-02-01
影响因子：
3.5
通讯作者：
Ueda, Hiroshi
中科院分区：
文献类型：
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作者：
Tsukahara, Ryoko;Yamamoto, Shinji;Ueda, Hiroshi
溶血磷脂酸 (LPA) 和 LPA1 受体信号传导通过疼痛相关基因/蛋白质表达和脱髓鞘的交替，在周围神经损伤诱发的神经性疼痛的引发中发挥着至关重要的作用。然而，人们对 LPA 及其在大脑中的信号传导仍然知之甚少。在本研究中，我们发现脱髓鞘开始后胼胝体中的 LPA5 受体表达升高，铜宗诱导脱髓鞘后通过 A δ 纤维产生的痛觉过敏是由 LPA5 信号介导的。这些数据表明 LPA5 信号传导可能在大脑脱髓鞘后神经性疼痛的机制中发挥关键作用。 (c) 2018 年作者。由 Elsevier B.V. 代表日本药理学会制作和主办。
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.