Hirst G D, Johnson S M, van Helden D F
J Physiol. 1985 Apr;361:315-37. doi: 10.1113/jphysiol.1985.sp015648.
Experiments were performed in current-clamped and voltage-clamped after-hyperpolarizing (AH) neurones of the guinea-pig myenteric plexus to examine the properties of the potassium conductance (gK, Ca) underlying the slow calcium-activated after-hyperpolarization (VK, Ca). The action potential plateau lengthened by the addition of tetraethylammonium chloride (TEA) to the bathing medium was compared to VK, Ca. Results were consistent with enhanced calcium entry causing an increase of VK, Ca. 4-Aminopyridine (4-AP) directly reduced VK, Ca. Voltage-clamp data of gK, Ca were well fitted by a process with a delay (approximately equal to 60 ms) followed by exponential activation (time constant approximately equal to 300 ms) and inactivation (time constant approximately equal to 2 s). The presence of a small, much slower inactivating process was noted. Values for time constants were similar to those reported by Morita, North & Tokimasa (1982) and North & Tokimasa (1983) where gK, Ca was measured during VK, Ca subsequent to action potential stimulation. The relation between gK, Ca (or the calcium-activated potassium current IK, Ca) and estimated calcium influx resulting from short-duration calcium currents elicited at various voltages was compared. Both the integral of the calcium current and gK, Ca showed a similar dependence on the depolarizations used to elicit IK, Ca except there was a positive shift of about 4 mV for the gK, Ca curve. This shift was attributed to a requirement for calcium ions to prime the gK, Ca mechanism. An inward ion charge movement of about 8 pC was required before significant activation of gK, Ca occurred. After the 'priming' condition had been established, the sensitivity of gK, Ca to inward calcium current measured at the resting potential was about 500 pS/pC of inward charge. Large calcium entry obtained by prolonged calcium currents caused saturation of the peak amplitude of IK, Ca and initiated currents with slower time to peak amplitude and longer duration. Increasing the calcium concentration of the external solution provided proportionally larger IK, Ca currents before saturation. The saturation amplitude of IK, Ca (namely gK, Ca) was relatively unaffected.
在豚鼠肠肌丛的电流钳制和电压钳制超极化后(AH)神经元中进行了实验,以研究慢钙激活超极化(VK, Ca)背后的钾电导(gK, Ca)特性。将向浴液中添加四乙铵氯化物(TEA)后延长的动作电位平台期与VK, Ca进行了比较。结果与钙内流增加导致VK, Ca增加一致。4-氨基吡啶(4-AP)直接降低了VK, Ca。gK, Ca的电压钳数据通过一个具有延迟(约60毫秒)、随后指数激活(时间常数约300毫秒)和失活(时间常数约2秒)的过程得到了很好的拟合。注意到存在一个小得多且失活较慢的过程。时间常数的值与森田、诺思和时正(1982年)以及诺思和时正(1983年)报道的值相似,他们在动作电位刺激后的VK, Ca期间测量了gK, Ca。比较了gK, Ca(或钙激活钾电流IK, Ca)与在不同电压下引发的短持续时间钙电流所导致的估计钙内流之间的关系。钙电流的积分和gK, Ca对用于引发IK, Ca的去极化显示出相似的依赖性,只是gK, Ca曲线有大约4毫伏的正移。这种移位归因于钙离子对gK, Ca机制的启动需求。在gK, Ca显著激活之前,需要约8皮库的内向离子电荷移动。在建立“启动”条件后,在静息电位下测量的gK, Ca对内向钙电流的敏感性约为每皮库内向电荷500皮秒。通过延长钙电流获得的大量钙内流导致IK, Ca的峰值幅度饱和,并引发峰值幅度时间较慢且持续时间较长的电流。增加外部溶液的钙浓度在饱和前提供了成比例更大的IK, Ca电流。IK, Ca的饱和幅度(即gK, Ca)相对不受影响。