Waxman Stephen G, Hains Bryan C
Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA.
Trends Neurosci. 2006 Apr;29(4):207-15. doi: 10.1016/j.tins.2006.02.003. Epub 2006 Feb 21.
Neuropathic pain and phantom phenomena occur commonly after spinal cord injury (SCI) but their molecular basis is not yet fully understood. Recent findings demonstrate abnormal expression of the Nav1.3 Na(+) channel within second-order spinal cord dorsal horn neurons and third-order thalamic neurons along the pain pathway after SCI, and suggest that this change makes these neurons hyperexcitable so that they act as pain amplifiers and generators. Delineation of molecular changes that contribute to hyperexcitability of pain-signaling neurons might lead to identification of molecular targets that will be useful in the treatment of neuropathic pain after SCI and related nervous system injuries.
神经性疼痛和幻肢现象在脊髓损伤(SCI)后很常见,但其分子基础尚未完全明确。最近的研究结果表明,SCI后,在疼痛传导通路中,脊髓背角二级神经元和丘脑三级神经元内Nav1.3钠通道表达异常,这表明这种变化使这些神经元过度兴奋,从而成为疼痛放大器和发生器。阐明导致疼痛信号神经元过度兴奋的分子变化,可能有助于确定对治疗SCI及相关神经系统损伤后神经性疼痛有用的分子靶点。