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P2X3受体介导的大鼠星状神经节神经元心肌缺血伤害性信号传导

Myocardial ischemic nociceptive signaling mediated by P2X3 receptor in rat stellate ganglion neurons.

作者信息

Zhang Chunping, Li Guilin, Liang Shangdong, Xu Changshui, Zhu Gaochun, Wang Yunxia, Zhang Aixia, Wan Fang

机构信息

Department of Physiology, Medical College of Nanchang University, Nanchang, Jiangxi 330006, PR China.

出版信息

Brain Res Bull. 2008 Jan 31;75(1):77-82. doi: 10.1016/j.brainresbull.2007.07.031. Epub 2007 Aug 28.

DOI:10.1016/j.brainresbull.2007.07.031
PMID:18158099
Abstract

Adenosine 5'-triphosphate (ATP) is implicated in peripheral pain signaling through activation of P2X receptors. P2X(3) receptors have a high level of expression in, and selective location on sensory afferents. P2X receptors, particularly the P2X(3) subtype, are identified as targets for novel analgesics. The stellate ganglion (SG) is peripheral sympathetic ganglia involved in heart function. Surgical interventions of sympathetic afferent pathways abolish or relieve angina pectoris, so it is showed that cardiac pain is mediated by the activation of afferents in sympathetic nerves. The cervicothoracic sympathetic ganglia, including the stellate ganglion, are implicated in sensations associated with myocardial ischemia or cardiac pain. In the present study we have examined P2X(3) involvement in cardiac nociceptive transmission. P2X receptor agonists activated currents (I(ATP)) in SG neurons. The I(ATP) amplitude and P2X(3) mRNA expression in myocardial ischemic injury group were much larger than those obtained in control group. Prostaglandin E(2) (PGE(2)) and substance P (SP) increased ATP-activated currents. P2X(3) receptor antagonist A-317491 reduced P2X agonist activated currents and P2X(3) mRNA expression. The results revealed that the myocardial ischemia induced the upregulation of P2X(3) receptor in function and morphous and P2X(3) receptor antagonist A-317491 inhibited P2X agonist activated currents and P2X(3) mRNA expression. The facts indicated that P2X(3) receptor in SG neurons was involved in cardiac nociceptive transmission.

摘要

三磷酸腺苷(ATP)通过激活P2X受体参与外周疼痛信号传导。P2X(3)受体在感觉传入神经中高水平表达且定位具有选择性。P2X受体,尤其是P2X(3)亚型,被确定为新型镇痛药的作用靶点。星状神经节(SG)是参与心脏功能的外周交感神经节。交感传入通路的外科干预可消除或缓解心绞痛,因此表明心脏疼痛是由交感神经传入神经的激活介导的。包括星状神经节在内的颈胸交感神经节与心肌缺血或心脏疼痛相关的感觉有关。在本研究中,我们检测了P2X(3)在心脏伤害性传递中的作用。P2X受体激动剂激活了星状神经节神经元中的电流(I(ATP))。心肌缺血损伤组的I(ATP)幅度和P2X(3)mRNA表达远大于对照组。前列腺素E2(PGE2)和P物质(SP)增加了ATP激活的电流。P2X(3)受体拮抗剂A-317491降低了P2X激动剂激活的电流和P2X(3)mRNA表达。结果显示,心肌缺血导致P2X(3)受体在功能和形态上上调,且P2X(3)受体拮抗剂A-317491抑制了P2X激动剂激活的电流和P2X(3)mRNA表达。这些事实表明,星状神经节神经元中的P2X(3)受体参与了心脏伤害性传递。

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