Calcium-dependent potassium currents in neurons from cat sensorimotor cortex.
Calcium-dependent potassium currents in neurons from cat sensorimotor cortex.
复制标题
猫感觉运动皮层神经元中的钙依赖性钾电流。
DOI：
10.1152/jn.1992.67.1.216
复制
发表时间：
1992
影响因子：
2.5
通讯作者：
Crill,WE
中科院分区：
文献类型：
--
作者：
Schwindt,PC;Spain,WJ;Crill,WE
1.采用体外脑片和单微电极电压钳技术，研究了猫感觉运动皮质V层大锥体神经元(Betz细胞)的钙依赖钾电流。以钙离子依赖性外向电流作为阻断钙内流前后的差值电流。在河豚毒素(TTX)存在的阶跃去极化过程中，这一电流表现出幅度可变的快速起始和显著的缓慢发展分量。2.当膜电位阶跃为-40 mV时，钙离子依赖性外向电流首次出现。从-40 mV的保持电位向下，几乎没有或几乎没有时间、电压或钙离子依赖的电流。当膜电位阶跃为-40 mV时，钙离子依赖的外向尾电流延长，随后出现复极化。该尾电流在-40 mV时的衰减可用时间常数为275+/-75(SD)ms的单一指数函数来描述。当胞外K+浓度([K+]o)为3 mM时，尾电流在96+/-5 mV处发生反转，并随着[K+]o的升高而出现正向电流，提示该电流主要由K+携带。3.钙依赖性钾电流由两个药理上可分离的成分组成。缓慢发展的电流对1 mM的四乙基铵(TEA)不敏感，但很大一部分被100 nM的阿帕明还原。加入异丙肾上腺素(20-50微米)或毒扁豆碱(10-20微米)可阻断大部分剩余电流。4.电压钳阶跃去极化激活时，氨基酸和递质敏感成分的时程相似，而在一系列动作电位激活时，两者的时程有很大不同。在90个棘波的末端施加电压钳(以100-200赫兹诱发)，产生钙依赖的钾电流，具有显著的快速衰减部分(在-mV时的时间常数约为50ms)和较小的缓慢衰减部分(时间常数在-mV时约为500ms)。阿帕明(50-200 nm)阻断快速衰退部分，异丙肾上腺素(20-50微米)阻断缓慢衰退部分。5.在含有2 mM二甲基双-(邻氨基苯氧基)-N，N，N‘，N’-四乙酸二甲酯(二甲基BAPTA)的微电极上记录时，阶跃去极化引起的钙依赖钾电流的起搏和衰减非常缓慢。在一系列诱发的尖峰之后记录到的电流也有类似的缓慢衰减。
1. Ca(2+)-dependent K+ currents were studied in large pyramidal neurons (Betz cells) from layer V of cat sensorimotor cortex by use of an in vitro brain slice and single microelectrode voltage clamp. The Ca(2+)-dependent outward current was taken as the difference current obtained before and after blockade of Ca2+ influx. During step depolarizations in the presence of tetrodotoxin (TTX), this current exhibited a fast onset of variable amplitude and a prominent slowly developing component. 2. The Ca(2+)-dependent outward current first appeared when membrane potential was stepped positive to -40 mV. Downsteps from a holding potential of -40 mV revealed little or no time-, voltage-, or Ca(2+)-dependent current. When membrane potential was stepped positive to -40 mV, a prolonged Ca(2+)-dependent outward tail current followed repolarization. The decay of this tail current at -40 mV was best described by a single exponential function having a time constant of 275 +/- 75 (SD) ms. The tail current reversed at 96 +/- 5 mV in 3 mM extracellular K+ concentration ([K+]o) and at more positive potentials when [K+]o was raised, suggesting that it was carried predominantly by K+. 3. The Ca(2+)-dependent K+ current consisted of two pharmacologically separable components. The slowly developing current was insensitive to 1 mM tetraethylammonium (TEA), but a substantial portion was reduced by 100 nM apamin. Most of the remaining current was blocked by the addition of isoproterenol (20-50 microM) or muscarine (10-20 microM). 4. The time courses of the apamin- and transmitter-sensitive components were similar when activated by step depolarizations in voltage clamp, but they were quite different when activated by a train of action potentials. Applying the voltage clamp at the end of a train of 90 spikes (evoked at 100-200 Hz) resulted in an Ca(2+)-dependent K+ current with a prominent rapidly decaying portion (time constant approximately 50 ms at -64 mV) and a smaller slowly decaying portion (time constant approximately 500 ms at -64 mV). The rapidly decaying portion was blocked by apamin (50-200 nM), and the slowly decaying portion was blocked by isoproterenol (20-50 microM). 5. When recorded with microelectrodes containing 2 mM dimethyl-bis-(o-aminophenoxy)-N,N,N',N'-tetraacetic acid (dimethyl-BAPTA), which causes prolonged afterhyperpolarizations, the Ca(2+)-dependent K+ current evoked by step depolarizations had an extremely slow onset and decay. The current recorded after a train of evoked spikes had a similar slow decay.(ABSTRACT TRUNCATED AT 400 WORDS)