颈上交感神经节细胞P2X_3受体介导心肌痛伤害性信息作用的电生理研究  

Eletrophysiology study of myocardial ischemic nociceptive signaling mediated by P2X_3 receptor in rat superior cervical ganglion neurons

作　　者：李桂林[1] 梁尚栋[1] 徐昌水[1] 高云[1] 许宝华[1] 张春平[1] 

机构地区：[1]南昌大学医学院生理学教研室,江西南昌330006

出　　处：《中国药理学通报》2007年第2期193-198,共6页Chinese Pharmacological Bulletin

基　　金：国家自然科学基金资助项目(No30460040)

摘　　要：目的观察心肌缺血致心肌痛伤害性剌激后颈上神经节(superior cervical ganglion,SCG)细胞P2X3受体在心肌痛伤害性信息传递中的作用。方法用全细胞膜片钳技术记录心肌缺血组和对照组大鼠新鲜分离的SCG神经元P2X受体激动剂激活电流及P2X3受体特异性拮抗剂A-317491对P2X受体激动剂激活电流的作用。结果①大部分受检细胞对ATP(1～1000μmol.L-1)敏感,ATP-激活电流(IATP)显示快失敏和慢失敏两种形式的内向电流,心肌缺血组IATP明显高于同一浓度时对照组的IATP。②在心肌缺血组SCG细胞,P2X3受体选择性激动剂α、β亚甲三磷酸腺苷(α,β-meATP)产生激活电流,而在对照组SCG细胞只有极少数细胞有此反应,且电流幅度小。③P2X3受体特异性拮抗剂A-317491(100nmol.L-1)对心肌缺血组和对照组ATP(100μmol.L-1)-激活电流均出现抑制作用,且同一浓度的A-317491对心肌缺血组IATP的抑制作用较对照组IATP的作用更为明显。A-317491(100nmol.L-1)使心肌缺血组和对照组SCG细胞α,β-meATP(10μmol.L-1)-激活电流减小,对心肌缺血组的抑制作用更明显。④心肌缺血组和对照组SCG细胞ATP(100μmol.L-1)-激活电流的I-U曲线反转电位不变,均接近0mV。结论心肌缺血后P2X受体激动剂在SCG神经元激活电流增大,P2X3受体特异性拮抗剂A-317491可抑制P2X受体激动剂激活的电流。因此,颈上交感神经节细胞的P2X3受体可能参与心肌痛伤害性感受信息的传递。Aim To explore effects of P2X3 receptor on myocardial ischemic nociceptive signaling in superior cervical ganglion （SCG） neurons. Methods P2X receptor agonist-activated currents and effects of A- 317491 on P2X receptor agonist-activated currents were studied by whole-cell patch-clamp technique in SCG neurons isolated from control and myocardial ischemic rats. Results （1） The majority of the SCG neurons in control group and SCG neurons in myocardial isehemie group were sensitive to ATP in the concentration range from 1 to 1000 μmol·L^-1. ATP evoked inward currents, which were categorized as rapid desensitization and slow desensitization. Amplitudes of the current in myocardial ischemic group were much larger than those obtained in control group after application of same concentration ATP. （2） α, β-meATP （ a selective agonist of P2X3 receptor） could induced currents in SCG neurons of myocardial ischemic rats, but only a little response in SCG neurons of control rats, and the amplitudes of latter were small. （3） A- 317491, a high affinity and selective antagonist ofP2X3, could inhibit ATP-activated currents in myocardial ischemic group and in control group; the inhibition of A-317491 was stronger in myocardial ischemic group than that in control group at the same concentration of A-317491. A-317491 （100 nmol·L^-1） reduced α, β-meATP （10 μmol·L^-1）-activated currents in myocardial ischemic group and in control group, the inhibition of A-317491 was much higher in myocardial ischemic group than that in control group. （4） There were no changes at the reversal potentials （0 mV） of ATP-activated currents in both groups. Conclusion P2X receptor agonist activated currents of SCG neurons were greatly potentiated after myocardial ischemia; A- 317491 could inhibit the currents activated by P2X receptors agonist. Therefore, P2X3 receptor in SCG neurons may be involved in the transmission of myocardial ischemic nociceptive signal.

关 键 词：三磷酸腺苷 P2X3 受体 心肌痛 颈上神经节 A-317491 全细胞膜片钳技术 

分 类 号：R-332[医药卫生] R322.11