Expression changes of cation chloride cotransporters in the rat spinal cord following intraplantar formalin
Expression changes of cation chloride cotransporters in the rat spinal cord following intraplantar formalin
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DOI：
10.1016/j.neures.2006.08.012
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发表时间：
2006-12-01
影响因子：
2.9
通讯作者：
Suzuki, Hidenori
中科院分区：
文献类型：
--
作者：
Nomura, Hidehiko;Sakai, Atsushi;Suzuki, Hidenori
据报道，氯离子阳离子共转运体，K+-Cl-共转运体2 （KCC2）和Na+-K+-Cl-共转运体1 （NKCC1）在脊髓神经元中表达并调节细胞内Cl-浓度。越来越多的证据表明，在炎症性或神经性疼痛中，氯离子共转运体的表达发生了变化，这种变化参与了持续疼痛状态的病理生理。然而，这些共转运蛋白如何在急性疼痛状态下促进痛觉过敏在很大程度上是未知的。因此，我们研究了大鼠足底注射福尔马林作为急性伤害性刺激后，KCC2和nkcc1在脊髓背角的表达变化。大鼠对福尔马林的反应表现出两个阶段（第一阶段和第二阶段）疼痛相关行为的增加。我们发现kcc2样免疫反应性（IR）在第一阶段在受刺激侧的腰椎I层和It层表达降低，然后逐渐恢复。相比之下，nkcc1样ir阳性细胞的数量在检查期间没有变化。这些结果表明，在福尔马林诱发痛觉过敏的初始阶段，KCC2而不是NKCC1主要参与调节脊髓背侧神经元的兴奋性。(c) 2006年爱思唯尔爱尔兰有限公司和日本神经科学学会。版权所有。
Cation chloride cotransporters, K+-Cl- cotransporter 2 (KCC2) and Na+-K+-Cl- cotransporter 1 (NKCC1) are reported to be expressed in the neurons in the spinal cord and regulate intracellular Cl- concentration. Evidence has been accumulating that the expression of cation chloride cotransporters changes in inflammatory or neuropathic pain, and such changes take a part in pathophysiology of the persistent pain states. However, it is largely unknown how these cotransporters contribute to hyperalgesia in the acute pain state. We, therefore, investigated expression changes of KCC2 and NKCC 1 in the spinal dorsal horn of the rat after the intraplantar injection of formalin as an acute nociceptive stimulus. The rats showed two phases (phases 1 and 2) of increase in pain-related behavior in response to formalin. We found that expression of KCC2-like immunoreactivity (IR) was reduced in lamina I and It in the lumbar spinal cord on the stimulated side in phase 1, and then recovered gradually. In contrast, the number of NKCC1-like IR-positive cells was unchanged over the period examined. These results suggest that KCC2, rather than NKCC1, mainly contributes to modulating excitability of the dorsal spinal cord neurons in the initial stage of formalin-evoked hyperalgesia. (c) 2006 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.