Belluzzi O, Sacchi O, Wanke E
J Physiol. 1985 Jan;358:91-108. doi: 10.1113/jphysiol.1985.sp015542.
Post-ganglionic neurones of the isolated rat superior cervical ganglion were voltage clamped at 37 degrees C using separate intracellular voltage and current micro-electrodes. Control experiments in current clamp suggested that the neurone is electrotonically compact, the soma and the proximal dendritic membranes being under good spatial voltage uniformity. Depolarizing voltage steps from membrane potentials near -50 mV evoked: (i) a voltage-dependent inward Na+ current, (ii) an inward Ca2+ current, (iii) a voltage-dependent outward K+ current, (iv) a Ca2+-activated K+ outward current. Depolarizations from holding potentials more negative than -60 mV elicited, besides the currents mentioned above, a fast transient outward current IA which peaked in 1-2.5 ms and then decayed to zero following an exponential time course. The IA current was shown to be primarily, if not exclusively, carried by K+. It was unaffected by removal of external Ca2+ or addition of Cd2+ and was weakly blocked by tetraethylammonium ions and partially by 4-aminopyridine. The IA current showed a linear instantaneous current-voltage relationship. Its activation ranged from -60 to 0 mV with a mid-point at -30 mV. The A conductance could be described in terms of a simple Boltzmann distribution for a single gating particle with a valency of +3. Both the development and removal of inactivation followed a single exponential time course with a voltage-dependent time constant which was large near the resting potential (42 ms at -70 mV) and small (11 ms) near -100 and -40 mV. Steady-state inactivation h infinity ranged from -100 to -50 mV, with a mid-point at -78 mV, suggesting that approximately 50% of the IA channels are available at the physiological resting potential. Action potentials elicited from various holding potentials showed maximal repolarization rates dependent on the holding potential itself. This voltage dependence was found to be in reasonably good agreement with that of h infinity curve. These data are consistent with the view that in the rat sympathetic neurone, under physiological conditions, it is the IA current rather than the delayed outward current that is responsible for the fast action potential repolarization.
使用单独的细胞内电压和电流微电极，在37℃对分离的大鼠颈上神经节的节后神经元进行电压钳制。电流钳制下的对照实验表明，该神经元在电紧张方面是致密的，其胞体和近端树突膜在空间电压上具有良好的均匀性。从接近 -50 mV的膜电位进行去极化电压阶跃可诱发：（i）电压依赖性内向Na⁺电流，（ii）内向Ca²⁺电流，（iii）电压依赖性外向K⁺电流，（iv）Ca²⁺激活的外向K⁺电流。从比 -60 mV更负的钳制电位进行去极化，除了上述电流外，还引发了一个快速瞬态外向电流IA，其在1 - 2.5 ms达到峰值，然后按照指数时间进程衰减至零。IA电流被证明主要（如果不是唯一）由K⁺携带。它不受去除细胞外Ca²⁺或添加Cd²⁺的影响，并且被四乙铵离子弱阻断，被4 - 氨基吡啶部分阻断。IA电流呈现线性瞬时电流 - 电压关系。其激活范围为 -60至0 mV，中点为 -30 mV。A电导可以用具有 +3价的单个门控粒子的简单玻尔兹曼分布来描述。失活的发展和去除均遵循单一指数时间进程，具有电压依赖性时间常数，该常数在静息电位附近较大（在 -70 mV时为42 ms），在 -100和 -40 mV附近较小（11 ms）。稳态失活h∞范围为 -100至 -50 mV，中点为 -78 mV，这表明在生理静息电位下约50%的IA通道是可用的。从各种钳制电位引发的动作电位显示出最大复极化速率取决于钳制电位本身。发现这种电压依赖性与h∞曲线的电压依赖性相当吻合。这些数据与以下观点一致，即在大鼠交感神经元中，在生理条件下，是IA电流而非延迟外向电流负责快速动作电位的复极化。
