Role of glia in neuropathic pain

Role of glia in neuropathic pain
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神经胶质细胞在神经性疼痛中的作用

DOI:
10.2741/4247
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发表时间:
2014-01-01
影响因子:
3.1
通讯作者:
Yuan, Hongbin
Yuan, Hongbin
中科院分区:
生物学4区
文献类型:
--
作者:
Liu, Fangting;Yuan, Hongbin

文献摘要

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神经性疼痛是由于疾病或身体损伤影响躯体感觉系统而引起的。它可以与异常感觉(感觉障碍)有关,也可以由正常的非疼痛刺激引起。神经胶质细胞已成为神经病理性痛觉的关键调节器和药物开发的潜在靶点。神经胶质细胞在周围神经损伤时被激活,并分泌许多促炎因子。这一过程涉及许多机制,包括神经炎症、离子通道激活和配体-受体相互作用。本文综述了神经病理性疼痛的最新研究进展,包括神经胶质细胞的作用以及当前治疗方法对其靶向性的影响。
Neuropathic pain is experienced as a result of disease or physical injury affecting the somatosensory system. It can be associated with abnormal sensations (dysesthesia) or evoked by normally nonpainful stimuli. Glia has emerged as key regulators of neuropathic pain perception and potential targets for drug development. Glia are activated upon peripheral nerve damage and secrete a number of proinflammatory factors. This process involves many mechanisms including neuroinflammation, ion channel activation, and ligand-receptor interactions. This review describes recent advances in the understanding of neuropathic pain, including the role of glia and their targeting by current treatment approaches.