肾上腺素引起牛蛙交感神经节神经元去极化的证据。

Evidence for epinephrine-induced depolarization in neurons of bullfrog sympathetic ganglia.

作者信息

Akasu T, Koketsu K

出版信息

Brain Res. 1987 Mar 10;405(2):375-9. doi: 10.1016/0006-8993(87)90309-x.

Abstract

The response to epinephrine (EP) was determined for neurons in bullfrog sympathetic ganglia by intracellular and voltage-clamp recording techniques. EP (5 microM-1 mM) produced a concentration-dependent depolarization mediated through beta-adrenoceptors. The EP-induced depolarization (EPD) was associated with a decrease in the membrane conductance. The EP-induced current (EP1) was decreased at hyperpolarizing potential levels and nullified at -70 mV. No reversal of the EPI polarity was seen. It is concluded that the EPD is generated by the suppression of a voltage-dependent gK, probably the M-channel.

摘要

通过细胞内和电压钳记录技术，测定了牛蛙交感神经节中神经元对肾上腺素（EP）的反应。EP（5微摩尔-1毫摩尔）通过β-肾上腺素能受体介导产生浓度依赖性去极化。EP诱导的去极化（EPD）与膜电导降低有关。EP诱导的电流（EP1）在超极化电位水平降低，并在-70毫伏时消失。未观察到EPI极性的反转。结论是，EPD是由电压依赖性gK（可能是M通道）的抑制产生的。