血管升压素对大鼠背根神经节神经元膜的作用
呼海燕, 孙志萍, 赵义梅, 司军强, 郑煜
石河子大学医学院生理教研室.新疆,石河子 832000;四川大学华西医学中心生理教研室.四川,成都 610041
摘要
为研究血管升压素(AVP)对大鼠背根神经节(DRG)神经元的作用及其机制,用细胞内微电极记录技术记录离体灌流DRG神经元的膜电位。结果如下:(1)在受检的120个细胞中,大多数(81.67%)在滴加AVP后产生明显的超极化反应。(2)滴加AVP(10#mu#mol/L)后膜电导增加约19.34%(P<0.05)。(3)灌流平衡液中的NaCl以氯化胆碱(CH-Cl)置代和用Cd~(2+)阻断Ca~(2+)通道后,AVP引起超极化反应的幅值均无明显变化(P>0.05),而加入K~(+)通道阻断剂四乙铵(TEA)后,AVP引起的超极化反应幅值明显减小(P<0.05)。(4)AVP引起的超极化反应可被AVP V_(1)受体拮抗剂阻断。结果提示,AVP可使DRG大多数神经元膜产生超极化,DRG神经元膜上存在AVP V_(1)受体,且AVP引起的超极化反应是通过神经元膜上AVP V_(1)受体介导的K~(+)外流所致,AVP可能参与了初级感受信息传入的调制。
关键词: 背根神经节; 细胞内记录; 血管升压素; 升压素受体
Effect of arginine vasopressin on membrane potential of dorsal root ganglion neurons in rats
Hu Haiyan, Sun Zhiping, Zhao Yimei, Si Junqiang, Zheng Yu
Department of Physiology,Shihezi University School of Medicine.Shihezi 832000,Xinjiang;China
Abstract
The results showed that (1) AVP induced hyperpolarization in the membrane of most DRG neurons. (2) The membrane conductance of the DRG neurons increased by 19.32% following application of AVP (P<0.05). (3) Perfusion with balance soldium solution (BSS) containing Cd~(2+) (blocker of Ca~(2+) channel) instead of Na~(+) failed to affect the AVP-induced membrane hyperpolarization of the DRG neurons (P>0.05). After perfusion with BSS containing tetraethylammonium (TEA), however, the extent of AVP-induced hyperpolarization was reduced (P<0.05). (4) The AVP-induced hyperpolarization of the neurons was blocked by the antagonist of AVP V_(1) receptors. The results demonstrate that AVP induces hyperpolarization of most DRG neurons, which might be caused by K~(+) outflow mediated by AVP V_(1) receptors in the membrane of the neurons.
Key words: dorsal root ganglion;intracellar recording;Arginine vasopressin;arginine vasopressin receptor
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引用本文:
呼海燕, 孙志萍, 赵义梅, 司军强, 郑煜. 血管升压素对大鼠背根神经节神经元膜的作用[J]. 生理学报 2004; 56 (1): .
Hu Haiyan, Sun Zhiping, Zhao Yimei, Si Junqiang, Zheng Yu. Effect of arginine vasopressin on membrane potential of dorsal root ganglion neurons in rats. Acta Physiol Sin 2004; 56 (1): (in Chinese with English abstract).