痛觉过敏的中枢敏感化机制及其分子基础

CENTRAL SENSITIZATION MECHANISM UNDERLYING HYPERALGESIA AND ITS MOLECULAR BASIS

摘要:

痛觉过敏一向被归咎于外周伤害性感受器的敏感化。新近有证据表明，中枢神经元的敏感化和高兴奋性在痛觉过敏的发生发展中具有至关重要的作用，并主要由ＮＭＤＡ受体－ＰＣＫ－ＮＯ等一系列受体－胞内分子过程参与。中枢敏感化及其分子基础的发现可望对疼痛临床防治提供新的对策。

Abstract:

Hyperalgesia has long time been attributed to sensitization of peripleral nociceptors. Sensitization and hyperexcitability of central neurons have now been demonstrated to play a critical role in initiation and maintenance of hyperalgesia; and a series of intracellular molecular events relating mainly to NMDA receptor-PKC-NO system is thought to involve in the development of hyperalgesia. Novel strategy for prevention and treatment of hyperalgesia is thus greatly expected based on the discovery of central sensitization and its molecular basis.