Evaluation of the analgesic effect to the neuropathic pain targeting ATP-sensitive potassium channels

尽管神经病理性疼痛的详细机制尚不清楚，但感觉功能的改变通过损伤轴突的过度兴奋性参与了神经病理性疼痛的发病。在此，我们研究了以ATP敏感性钾通道为靶点的神经病理性疼痛的镇痛作用。我们的结果表明，K_ATP电流的减少可能是通过增加兴奋性而产生神经病理性疼痛的一个因素。此外，我们还探讨了神经类固醇作为调节K_ATP通道活性的内源性因子的可能性。我们的结果表明，别孕酮是一种神经类固醇，在神经病理性疼痛的发病机制中起作用。

Although detailed mechanisms of neuropathic pain remained unclear, altered sensory function contributes to the pathogenesis of neuropathic pain via hyperexcitability in injured axons. Here, we investigated the analgesic effect to the neuropathic pain targeting ATP-sensitive potassium(K_<ATP>) channels. Our results indicated that reduced K_ATP currents may be a factor in generating neuropathic pain through increased excitability. In addition, we examined the possibility of neurosteroid as the endogenous factor which can modulate K_ATP channel activity. Our results demonstrated that allopregnanolone, one of the neurosteroid, contributed to the pathogenesis of neuropathic pain.