Hu Hai-Yan, Sun Zhi-Ping, Zhao Yi-Mei, Si Jun-Qiang, Zheng Yu
Department of Physiology, Shihezi University School of Medicine, Shihezi 832000, Xinjiang, China.
Sheng Li Xue Bao. 2004 Feb 25;56(1):107-11.
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 sodium 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.
采用细胞内记录技术,在大鼠中研究了精氨酸加压素(AVP)对背根神经节(DRG)神经元膜电位的影响。结果表明:(1)AVP可使大多数DRG神经元的膜发生超极化。(2)应用AVP后,DRG神经元的膜电导增加了19.32%(p<0.05)。(3)用含镉(2+)(钙通道阻滞剂)的平衡钠溶液(BSS)代替钠进行灌注,未能影响AVP诱导的DRG神经元膜超极化(p>0.05)。然而,用含四乙铵(TEA)的BSS灌注后,AVP诱导的超极化程度降低(p<0.05)。(4)AVP诱导的神经元超极化被AVP V(1)受体拮抗剂阻断。结果表明,AVP可使大多数DRG神经元超极化,这可能是由神经元膜上AVP V(1)受体介导的钾离子外流所致。