血管升压素对大鼠背根神经节神经元膜的作用

为研究血管升压素(arginine vasopressin,AVP)对大鼠背根神经节(dorsal root ganglion,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(10μmol/L)后膜电导增加约19.34％(P<0.05)。(3)灌流平衡液巾的NaCl以氯化胆碱(CH-Cl)置代和用Cd2+阻断Ca2+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.受体拈抗剂阻断。结果捉示,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,受体,且AVP引起的超极化反应是通过神经元膜上AVP V.受体介导的K+外流所致.AVP可能参与了初级感觉信息传入的调制。

Effect of arginine vasopressin on membrane potential of dorsal root ganglion neurons in rats

The effect of arginine vasopressin (AVP) on membrane potential of neurons from dorsal root ganglion (DRG) was examined in the rat by means of intracellular recording technique. 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 Cd2+ (blocker of Ca2+ 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 V1receptors. The results demonstrate that AVP induces hyperpolarization of most DRG neurons, which might be caused by K+ outflow mediated by AVP V1 receptors in the membrane of the neurons.