Voltage-gated transient currents in bovine adrenal fasciculata cells. II. A-type K+ current.
Voltage-gated transient currents in bovine adrenal fasciculata cells. II. A-type K+ current.
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DOI：
10.1085/jgp.102.2.239
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发表时间：
1993-08
期刊：
影响因子：
--
通讯作者：
Enyeart JJ
中科院分区：
文献类型：
--
作者：
Mlinar B;Enyeart JJ
在全细胞膜片钳记录酶促解离的肾上腺束状细胞（AZF）上，在150多个细胞中的每一个中观察到快速失活的A型K+电流。IA的激活是急剧的电压依赖性的，并且可以通过提高到4的整数幂的Boltzmann函数来描述，中点为-28.3mV。使用"极限对数电位灵敏度"，估计单通道门控电荷为7.2 e。电压依赖性失活也可以用Boltzmann函数描述，中点为-58.7 mV，斜率因子为5.92 mV。IA的门控动力学包括闭合、开放和失活状态之间通路的电压依赖性和非依赖性转变。IA激活与电压依赖性S形动力学，可以与n4h形式主义。激活时间常数τ a在电位为0 mV时达到一个与电压无关的最小值. IA电流失活的两个时间常数是电压无关的电位范围从-30到+45 mV。在+20 mV时，tau i（快）和tau i（慢）分别为13.16 +/-0.64和62.26 +/-5.35 ms（n = 34）。在一些细胞中，IA失活动力学在全细胞记录许多分钟后显著减慢。一旦被去极化激活，IA通道就沿着沿着通道恢复到关闭状态，在-80 mV时具有两个电压依赖性时间常数，分别为0.208 s，tau rec-f和10.02 s，tau rec-s。在-60 mV和-100 mV之间的电位下，约90%的IA电流以缓慢的动力学恢复。IA被4-氨基吡啶（IC50 = 629 μ M）通过通道激活强烈促进的机制阻断。包括Ni 2+和La 3+的二价和三价阳离子也分别以467和26.4 μ M的IC 50阻断IA。关于生物物理性质和药理学，AZF细胞中的IA在某种程度上类似于神经元和肌肉中的瞬时K+电流，它们的功能是调节动作电位频率和持续时间。这种不产生动作电位的内分泌细胞在类固醇激素分泌中的作用尚不清楚。
In whole cell patch clamp recordings on enzymatically dissociated adrenal zona fasciculata (AZF) cells, a rapidly inactivating A-type K+ current was observed in each of more than 150 cells. Activation of IA was steeply voltage dependent and could be described by a Boltzmann function raised to an integer power of 4, with a midpoint of -28.3 mV. Using the "limiting logarithmic potential sensitivity," the single channel gating charge was estimated to be 7.2 e. Voltage-dependent inactivation could also be described by a Boltzmann function with a midpoint of -58.7 mV and a slope factor of 5.92 mV. Gating kinetics of IA included both voltage-dependent and -independent transitions in pathways between closed, open, and inactivated states. IA activated with voltage-dependent sigmoidal kinetics that could be fit with an n4h formalism. The activation time constant, tau a, reached a voltage- independent minimum at potentials positive to 0 mV. IA currents inactivated with two time constants that were voltage independent at potentials ranging from -30 to +45 mV. At +20 mV, tau i(fast) and tau i(slow) were 13.16 +/- 0.64 and 62.26 +/- 5.35 ms (n = 34), respectively. In some cells, IA inactivation kinetics slowed dramatically after many minutes of whole cell recording. Once activated by depolarization, IA channels returned to the closed state along pathways with two voltage-dependent time constants which were 0.208 s, tau rec-f and 10.02 s, tau rec-s at -80 mV. Approximately 90% of IA current recovered with slow kinetics at potentials between -60 and -100 mV. IA was blocked by 4-aminopyridine (IC50 = 629 microM) through a mechanism that was strongly promoted by channel activation. Divalent and trivalent cations including Ni2+ and La3+ also blocked IA with IC50's of 467 and 26.4 microM, respectively. With respect to biophysical properties and pharmacology, IA in AZF cells resembles to some extent transient K+ currents in neurons and muscle, where they function to regulate action potential frequency and duration. The function of this prominent current in steroid hormone secretion by endocrine cells that may not generate action potentials is not yet clear.