Smith P A
J Physiol. 1984 Feb;347:377-95. doi: 10.1113/jphysiol.1984.sp015071.
The effect of adrenaline and acetylcholine (ACh) on the membrane potential of Rana pipiens sympathetic ganglia was examined by means of the sucrose gap recording technique. Adrenaline (1-50 microM) consistently produced a hyperpolarization (Adrh) which was not reduced by Ringer solution containing 10 mM-Mn2+, nor by Ringer solution where the Na+ concentration was reduced from 100 to 30 mM. High doses of ACh (10 mM) produced a biphasic response, a depolarization (AChd) followed by an after-hyperpolarization (ACha.h.p.). Ringer solution containing 100 mM-Li+ (rather than 100 mM-Na+) or 10 microM-ouabain blocked the ACha.h.p. and reduced the Adrh. The AChd was essentially unchanged. Ringer solution containing 0.2 mM-K+ (rather than 2 mM-K+) blocked part of the ACha.h.p. whereas the Adrh was enhanced. Ringer solution containing 6 mM-K+ reduced the amplitude of the Adrh. The Adrh and the antidromically evoked action potential after-hyperpolarization (antidromic a.h.p.) reversed polarity at approximately the same membrane potential. These data do not support the hypothesis that the Adrh results from activation of the electrogenic sodium pump. It is tempting to speculate that the response may be generated by an increase in potassium conductance (gK) which is especially sensitive to manipulations which result in sodium pump inhibition.
采用蔗糖间隙记录技术研究了肾上腺素和乙酰胆碱（ACh）对牛蛙交感神经节膜电位的影响。肾上腺素（1 - 50微摩尔）始终产生超极化（Adrh），含10毫摩尔 - Mn²⁺的林格溶液或Na⁺浓度从100毫摩尔降至30毫摩尔的林格溶液均不能使其降低。高剂量的ACh（10毫摩尔）产生双相反应，先是去极化（AChd），随后是后超极化（ACha.h.p.）。含100毫摩尔 - Li⁺（而非100毫摩尔 - Na⁺）或10微摩尔哇巴因的林格溶液可阻断ACha.h.p.并降低Adrh。AChd基本未变。含0.2毫摩尔 - K⁺（而非2毫摩尔 - K⁺）的林格溶液可阻断部分ACha.h.p.，而Adrh增强。含6毫摩尔 - K⁺的林格溶液可降低Adrh的幅度。Adrh和逆向诱发动作电位后超极化（逆向a.h.p.）在大致相同的膜电位处反转极性。这些数据不支持Adrh是由生电钠泵激活所致的假说。很容易推测该反应可能是由钾电导（gK）增加产生的，钾电导对导致钠泵抑制的操作特别敏感。
