Akasu T, Koketsu K
Jpn J Physiol. 1976;26(3):289-301. doi: 10.2170/jjphysiol.26.289.
Effects of adrenaline on K+ -activated hyperpolarization of bullfrog sympathetic ganglion cells, preganglionic nerve axons and splanchnic nerve axons were studied. The K+ -activated hyperpolarization recorded from ganglion-postgangaline (0.3 mM). On the other hand, the K+ -activated hyperpolarization of postganglionic, preganglionic nerve axons and splanchnic nerve axons was not affected under the same experimental conditions. The facil-tatory effect of adrenaline on the K+ -activated hyperpolization was gradually intensified when the application of adrenaline was sustained for up to 60 min. The effect was reversible. The K+ -activated hyperpolarization recorded from ganglion cell-bodies by intracellular microelectrodes was similarly augmented by adrenaline (0.1 mM). Adrenaline in this concentration, however, caused no significant changes of the membrane potential and conductance in the presence of ouabain (0.002 mM) which completely and reversibly inhibited K+-activated hyperpolarization. Noradrenaline showed similar but less effected and isoproterenol showed no significant effect on the K+ -activated hyperpolarization. The facilitatory effect of adrenaline was inhibited in the presence of phentolamine but not of DCI. These results suggested that the intraganglionic membrane of ganglion cells possessed some kind of adrenergic alpha-receptors and the electrogenic Na+ pump of ganglion cells was accelerated by some unknown mechanism when adrenaline reacted to these receptors.
研究了肾上腺素对牛蛙交感神经节细胞、节前神经轴突和内脏神经轴突钾离子激活超极化的影响。在神经节 - 节后神经（0.3 mM）处记录到钾离子激活超极化。另一方面，在相同实验条件下，节后、节前神经轴突和内脏神经轴突的钾离子激活超极化不受影响。当持续应用肾上腺素长达60分钟时，肾上腺素对钾离子激活超极化的促进作用逐渐增强。该作用是可逆的。通过细胞内微电极从神经节细胞体记录到的钾离子激活超极化同样被肾上腺素（0.1 mM）增强。然而，在存在哇巴因（0.002 mM）的情况下，该浓度的肾上腺素并未引起膜电位和电导的显著变化，哇巴因完全且可逆地抑制钾离子激活超极化。去甲肾上腺素表现出类似但作用较小的效果，而异丙肾上腺素对钾离子激活超极化无显著影响。在酚妥拉明存在时，肾上腺素的促进作用受到抑制，但在DCI存在时则不受影响。这些结果表明，神经节细胞的神经节内细胞膜具有某种肾上腺素能α受体，当肾上腺素与这些受体反应时，神经节细胞的电生性钠泵通过某种未知机制被加速。
