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

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• 作者：Chunping Zhang ; Guilin Li ; Shangdong Liang ; Changshui Xu ; Gaochun Zhu ; Yunxia Wang ; Aixia Zhang ; Fang Wan
• 关键词：ATP ; P2X₃ receptor ; A-317491 ; Stellate ganglion ; Myocardial ischemia
• 刊名：Brain Research Bulletin
• 出版年：2008
• 期刊代码：9_03619230
• 类别：neu
• 出版时间：31 January 2008
• 卷：75
• 期：1
• 页码：77-82
• 文件大小：452 K

摘要

Adenosine 5′-triphosphate (ATP) is implicated in peripheral pain signaling through activation of P2X receptors. P2X₃ receptors have a high level of expression in, and selective location on sensory afferents. P2X receptors, particularly the P2X₃ 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 P2X₃ involvement in cardiac nociceptive transmission. P2X receptor agonists activated currents (I_ATP) in SG neurons. The I_ATP amplitude and P2X₃ mRNA expression in myocardial ischemic injury group were much larger than those obtained in control group. Prostaglandin E₂ (PGE₂) and substance P (SP) increased ATP-activated currents. P2X₃ receptor antagonist A-317491 reduced P2X agonist activated currents and P2X₃ mRNA expression. The results revealed that the myocardial ischemia induced the upregulation of P2X₃ receptor in function and morphous and P2X₃ receptor antagonist A-317491 inhibited P2X agonist activated currents and P2X₃ mRNA expression. The facts indicated that P2X₃ receptor in SG neurons was involved in cardiac nociceptive transmission.