Electrophysiological studies of upregulated P2X7 receptors in rat superior cervical ganglia after myocardial ischemic injury
Electrophysiological studies of upregulated P2X7 receptors in rat superior cervical ganglia after myocardial ischemic injury
复制标题
心肌缺血损伤后大鼠颈上神经节P2X7受体上调的电生理研究
DOI：
10.1016/j.neuint.2013.06.003
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发表时间：
2013-09-01
影响因子：
4.2
通讯作者：
Liang, Shangdong
中科院分区：
文献类型：
--
作者：
Kong, Fanjun;Liu, Shuangmei;Liang, Shangdong
心肌缺血性损伤激活心脏交感传入纤维，通过兴奋交感传出作用引起交感兴奋性反射，从而增加心肌耗氧量，导致加重心肌缺血的恶性循环。P2 X（7）受体参与神经元功能和神经系统疾病。本研究探讨了上级颈神经节（SCG）P2 X（7）受体在交感神经兴奋反射中的作用。结果表明，心肌缺血损伤后，SCG中P2 X（7）受体mRNA和蛋白表达均增加。相同浓度的P2 X（7）受体激动剂在心肌缺血大鼠的SCG神经元上激活的电流幅度远大于对照组。P2 X（7）受体拮抗剂（brilliant blue G，BBG）显著抑制P2 X（7）受体激动剂激活的电流。P2 X（7）受体激活后MAPK/ERK 1/2的过度磷酸化可能是介导心肌缺血损伤后信号转导的机制之一。因此，SCG上敏感的P2 X（7）受体参与了心肌缺血损伤引起的交感兴奋反射的伤害性传递。(C)2013爱思唯尔有限公司保留所有权利。
Myocardial ischemic injury activates cardiac sympathetic afferent fibers and elicits a sympathoexcitatory reflex by exciting sympathetic efferent action, with resultant augmentation of myocardial oxygen consumption, leading to a vicious cycle of exaggerating myocardial ischemia. P2X(7) receptor participates in the neuronal functions and the neurological disorders. This study examined the role of P2X(7) receptor of superior cervical ganglia (SCG) in sympathoexcitatory reflex. Our results showed that the expression of P2X(7) receptor at both mRNA and protein in SCG was increased after myocardial ischemic injury. P2X(7) receptor agonists at the same concentration activated much larger amplitudes of the currents in the SCG neurons of myocardial ischemic rats than those in control rats. P2X(7) receptor antagonist (brilliant blue G, BBG) significantly inhibited P2X(7) receptor agonist-activated currents in the SCG neurons. Excessive phosphorylation of MAPK ERK1/2 upon the activation of P2X(7) receptor might be a mechanism mediating the signal transduction after myocardial ischemic injury. Therefore, the sensitized P2X(7) receptor in SCG was involved in the nociceptive transmission of sympathoexcitatory reflex induced by myocardial ischemic injury. (C) 2013 Elsevier Ltd. All rights reserved.