Madison D V, Nicoll R A
J Physiol. 1984 Sep;354:319-31. doi: 10.1113/jphysiol.1984.sp015378.
Experiments using intracellular recording techniques were performed on rat hippocampal neurones in vitro, to study the discharge properties of these cells. When CA 1 pyramidal cells were excited by injecting long depolarizing current pulses (approximately 600-800 ms), they responded with an initial rapid action potential discharge which slowed, or accommodated, and then stopped after 200-300 ms. The train of action potentials was followed by a hyperpolarization which was due primarily to calcium-activated potassium conductance (GK(Ca]. The amplitude of this hyperpolarization increased with an increasing number of action potentials in the initial discharge. Blocking the calcium-activated potassium conductance, by injecting EGTA into the cell, by bathing the cell in cadmium, a calcium channel blocker, or by bathing the cell in calcium-free medium, reduced the after-hyperpolarization (a.h.p.) and accommodation such that the frequency of action potential discharge increased and the duration of this discharge was prolonged. Blocking the calcium-activated potassium conductance had a greater effect on discharge frequency later in the action potential train, as late interspike intervals were shortened more than early ones by the application of cadmium or of calcium-free medium. This was presumably because the calcium-activated potassium conductance was more developed later in the train. Accommodation was not completely abolished in the absence of calcium and presence of cadmium, suggesting that other factors, in addition to calcium-activated potassium conductance, contributed to this process. This remaining accommodation was reduced by low doses of carbachol, suggesting that the M-current also plays a role in accommodation. We conclude that accommodation of the action potential discharge of hippocampal pyramidal cells may be regulated by at least two potassium currents: the calcium-activated potassium current and the M-current. Both of these currents are turned on during excitation of the neurone and act in an inhibitory manner on that neurone to limit further action potential discharge.
利用细胞内记录技术对体外培养的大鼠海马神经元进行了实验，以研究这些细胞的放电特性。当通过注入长时去极化电流脉冲（约600 - 800毫秒）刺激CA1锥体细胞时，它们会以最初的快速动作电位放电做出反应，随后放电减慢或适应，然后在200 - 300毫秒后停止。动作电位序列之后是超极化，这主要是由于钙激活钾电导（GK(Ca]）所致。这种超极化的幅度随着初始放电中动作电位数量的增加而增大。通过向细胞内注入乙二醇双四乙酸（EGTA）、将细胞置于钙通道阻滞剂镉中或无钙培养基中，阻断钙激活钾电导，可减少后超极化（a.h.p.）和适应现象，使得动作电位放电频率增加且放电持续时间延长。阻断钙激活钾电导对动作电位序列后期的放电频率影响更大，因为应用镉或无钙培养基后，后期的峰间间隔比早期的缩短得更多。这可能是因为钙激活钾电导在序列后期更为发达。在无钙和有镉存在的情况下，适应现象并未完全消除，这表明除了钙激活钾电导外，其他因素也参与了这一过程。低剂量的卡巴胆碱可减少这种剩余的适应现象，这表明M电流在适应过程中也起作用。我们得出结论，海马锥体细胞动作电位放电的适应可能至少受两种钾电流调节：钙激活钾电流和M电流。这两种电流在神经元兴奋时开启，并以抑制方式作用于该神经元，以限制进一步的动作电位放电。
