Neuron-glia crosstalk gets serious: role in pain hypersensitivity.
Neuron-glia crosstalk gets serious: role in pain hypersensitivity.
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DOI：
10.1097/aco.0b013e32830edbdf
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发表时间：
2008-10
期刊：
影响因子：
--
通讯作者：
Dubner R
中科院分区：
文献类型：
--
作者：
Ren K;Dubner R
最近的研究表明，外周损伤激活外周和中枢细胞回路的神经元和非神经元或神经胶质成分。随后的神经元-胶质细胞相互作用导致疼痛超敏反应。这篇综述将简要讨论新的发现，揭示了持续性疼痛中神经元-胶质细胞相互作用的细胞机制。与疼痛机制中神经元-胶质细胞相互作用相关的两个基本问题已经得到解决：1）损伤后导致中枢胶质细胞激活的信号是什么; 2）胶质细胞如何影响CNS神经元活性并促进痛觉过敏。有证据表明，中央胶质细胞的激活依赖于损伤部位的神经输入和化学介质的释放。血原性免疫细胞可迁移/浸润至脑，并且循环炎性介质可穿透血脑屏障以参与对损伤的中枢神经胶质反应。从胶质细胞释放的炎性细胞因子如IL-1β可能通过其与神经元谷氨酸受体的偶联促进疼痛传递。这种双向神经元-胶质细胞信号传导在胶质细胞活化、细胞因子产生以及痛觉过敏的启动和维持中起关键作用。认识到神经元-胶质细胞相互作用对中枢致敏和痛觉过敏的贡献，提示了慢性疼痛的新治疗方法。
Recent studies show that peripheral injury activates both neuronal and non-neuronal or glial components of the peripheral and central cellular circuitry. The subsequent neuron-glial interactions contribute to pain hypersensitivity. This review will briefly discuss novel findings that have shed light on the cellular mechanisms of neuron-glial interactions in persistent pain. Two fundamental questions related to neuron-glial interactions in pain mechanisms have been addressed: 1) what are the signals that lead to central glial activation after injury and 2) how glial cells affect CNS neuronal activity and promote hyperalgesia. Evidence indicates that central glial activation depends on nerve inputs from the site of injury and release of chemical mediators. Hematogenous immune cells may migrate/infiltrate to the brain and circulating inflammatory mediators may penetrate the blood brain barrier to participate in central glial responses to injury. Inflammatory cytokines such as IL-1β released from glia may facilitate pain transmission through its coupling to neuronal glutamate receptors. This bidirectional neuron-glial signaling plays a key role in glial activation, cytokine production and the initiation and maintenance of hyperalgesia. Recognition of the contribution of the mutual neuron-glial interactions to central sensitization and hyperalgesia prompts new treatment for chronic pain.