Lynch J W, Barry P H
School of Physiology and Pharmacology, University of New South Wales, Sydney, Australia.
J Gen Physiol. 1991 May;97(5):1043-72. doi: 10.1085/jgp.97.5.1043.
The transient potassium current, IK(t), of enzymatically dissociated rat olfactory receptor neurons was studied using patch-clamp techniques. Upon depolarization from negative holding potentials, IK(t) activated rapidly and then inactivated with a time course described by the sum of two exponential components with time constants of 22.4 and 143 ms. Single-channel analysis revealed a further small component with a time constant of several seconds. Steady-state inactivation was complete at -20 mV and completely removed at -80 mV (midpoint -45 mV). Activation was significant at -40 mV and appeared to reach a maximum conductance at +40 mV (midpoint -13 mV). Deactivation was described by the sum of two voltage-dependent exponential components. Recovery from inactivation was extraordinarily slow (50 s at -100 mV) and the underlying processes appeared complex. IK(t) was reduced by 4-aminopyridine and tetraethylammonium applied externally. Increasing the external K+ concentration ([K+]o) from 5 to 25 mM partially removed IK(t) inactivation, usually without affecting activation kinetics. The elevated [K+]o also hyperpolarized the steady-state inactivation curve by 9 mV and significantly depolarized the voltage dependence of activation. Single transient K+ channels, with conductances of 17 and 26 pS, were observed in excised patches and often appeared to be localized into large clusters. These channels were similar to IK(t) in their kinetic, pharmacological, and voltage-dependent properties and their inactivation was also subject to modulation by [K+]o. The properties of IK(t) imply a role in action potential repolarization and suggest it may also be important in modulating spike parameters during neuronal burst firing. A simple method is also presented to correct for errors in the measurement of whole-cell resistance (Ro) that can result when patch-clamping very small cells. The analysis revealed a mean corrected Ro of 26 G omega for these cells.
采用膜片钳技术研究了酶解大鼠嗅觉受体神经元的瞬时钾电流(IK(t))。从负的钳制电位去极化时,IK(t)迅速激活,然后失活,其时间进程由两个时间常数分别为22.4和143毫秒的指数成分之和描述。单通道分析揭示了一个时间常数为几秒的更小成分。稳态失活在-20 mV时完成,在-80 mV时完全消除(中点为-45 mV)。激活在-40 mV时显著,在+40 mV时似乎达到最大电导(中点为-13 mV)。失活由两个电压依赖性指数成分之和描述。从失活状态恢复非常缓慢(在-100 mV时为50秒),其潜在过程似乎很复杂。外部施加4-氨基吡啶和四乙铵可使IK(t)减小。将外部钾离子浓度([K+]o)从5 mM增加到25 mM可部分消除IK(t)的失活,通常不影响激活动力学。升高的[K+]o还使稳态失活曲线超极化9 mV,并显著使激活的电压依赖性去极化。在切除的膜片中观察到电导为17和26 pS的单个瞬时钾通道,它们常常似乎聚集形成大的簇。这些通道在动力学、药理学和电压依赖性特性方面与IK(t)相似,其失活也受[K+]o的调节。IK(t)的特性表明它在动作电位复极化中起作用,并提示它在调节神经元爆发式放电期间的峰电位参数方面可能也很重要。还提出了一种简单方法来校正膜片钳非常小的细胞时可能导致的全细胞电阻(Ro)测量误差。分析显示这些细胞的平均校正Ro为26 GΩ。