Zhang Xu, Xiao Hua-Sheng
Chinese Academy of Sciences, Shanghai Institutes for Biological Sciences, Institute of Neurosciences, Laboratory of Sensory System, Shanghai 200031, PR China.
Curr Opin Mol Ther. 2005 Dec;7(6):532-7.
The molecular modification of the pain pathway represents one of the major mechanisms underlying neuropathic pain. Recently, gene array studies have been carried out to identify the genes that are regulated at the spinal cord level after peripheral nerve injury. These studies demonstrate that peripheral nerve injury causes marked changes in gene expression in both the dorsal root ganglion (DRG) and the dorsal spinal cord. The markedly regulated molecules include, for example, neuropeptides, receptors, ion channels, signal transduction molecules and synaptic vesicle proteins. Upregulation of the Ca2+ channel alpha2/delta1 subunit, gamma-aminobutyric acid A receptor alpha5 subunit, Na+ channels and nicotinic acetylcholine receptors in the DRG and dorsal spinal cord indicates their potential roles in neuropathic pain control.
疼痛通路的分子修饰是神经性疼痛的主要潜在机制之一。最近，人们开展了基因阵列研究，以确定外周神经损伤后在脊髓水平受到调控的基因。这些研究表明，外周神经损伤会导致背根神经节（DRG）和脊髓背角的基因表达发生显著变化。显著受调控的分子包括神经肽、受体、离子通道、信号转导分子和突触小泡蛋白等。DRG和脊髓背角中钙离子通道α2/δ1亚基、γ-氨基丁酸A受体α5亚基、钠离子通道和烟碱型乙酰胆碱受体的上调表明它们在神经性疼痛控制中具有潜在作用。
