小胶质细胞-神经元信号在神经病理性疼痛超敏反应 2.0 中的作用
Microglia-neuronal signalling in neuropathic pain hypersensitivity 2.0.
机构信息
Program in Neurosciences & Mental Health, Hospital for Sick Children, 555 University Avenue, Toronto, ON M6H 2X6, Canada.
出版信息
Curr Opin Neurobiol. 2010 Aug;20(4):474-80. doi: 10.1016/j.conb.2010.08.005.
Abstract
Microglia are increasingly recognized as critical in the pathogenesis of pain hypersensitivity caused by injury to peripheral nerves. The core signalling pathway is through P2X4 purinergic receptors on the microglia which, via the release of brain-derived neurotrophic factor, cause disinhibition of nociceptive dorsal horn neurons by raising intracellular chloride levels. This disinhibition works in synergy with enhanced excitatory synaptic transmission in the dorsal horn to transform the output of the nociceptive network. There is increased discharge output, unmasking of responses to innocuous peripheral inputs and spontaneous activity in neurons that otherwise only signal nociception. Together the changes caused by microglia-neuron signalling may account for the main symptoms of neuropathic pain in humans.
摘要
小胶质细胞在由周围神经损伤引起的痛觉过敏发病机制中越来越受到重视。核心信号通路是通过小胶质细胞上的 P2X4 嘌呤能受体，通过释放脑源性神经营养因子，导致伤害性背角神经元去抑制，通过提高细胞内氯离子水平。这种去抑制与背角中增强的兴奋性突触传递协同作用，改变伤害性网络的输出。放电输出增加，掩盖了对无害外周输入的反应，以及原本只传递伤害性信号的神经元的自发性活动。小胶质细胞-神经元信号引起的变化可能解释了人类神经性疼痛的主要症状。
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