CONTROL OF THE REPETITIVE DISCHARGE OF RAT CA1 PYRAMIDAL NEURONS INVITRO
CONTROL OF THE REPETITIVE DISCHARGE OF RAT CA1 PYRAMIDAL NEURONS INVITRO
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DOI：
10.1113/jphysiol.1984.sp015378
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发表时间：
1984-01-01
影响因子：
5.5
通讯作者：
NICOLL, RA
中科院分区：
文献类型：
--
作者：
MADISON, DV;NICOLL, RA
使用细胞内记录技术对体外大鼠海马神经元进行实验，以研究这些细胞的放电特性。当通过注入长去极化电流脉冲（约600-800毫秒）来激发CA 1锥体细胞时，它们以最初的快速动作电位放电做出反应，该放电减慢或适应，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 Ca 激活的 K 电导 (GK(Ca))。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加。通过将EGTA[乙二醇-双(β-氨基乙基醚)N,N,N,N''-四乙酸]注射到细胞中，通过将细胞浸泡在Ca通道阻断剂Cd中，或将细胞浸泡在无Ca培养基中，阻断Ca激活的K电导，减少后超极化(a.h.p.)和调节，使得动作电位放电的频率增加并且该放电的持续时间延长。阻断 Ca 激活的 K 电导对动作电位序列后期的放电频率有更大的影响，因为通过应用 Cd 或不含 Ca 的介质，后期的尖峰间隔比早期的尖峰间隔缩短得更多。这可能是因为 Ca 激活的 K 电导在列车后期得到了进一步发展。在没有 Ca 且存在 Cd 的情况下，调节并没有完全消除，这表明除了 Ca 激活的 K 电导之外，其他因素也促成了这一过程。低剂量的卡巴胆碱减少了剩余的调节，表明 M 电流也在调节中发挥作用。海马锥体细胞动作电位放电的调节可以通过至少 2 K 电流来调节：Ca 激活 K 电流和 M 电流。这两个电流在神经元兴奋期间打开，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。
Experiments using intracellular recording techniques were performed on rat hippocampal neurons in vitro, to study the discharge properties of these cells. When CA 1 pyramidal cells were excited by injecting long depolarizing current pulses (.apprx. 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 Ca-activated K conductance (GK(Ca)). The amplitude of this hyperpolarization increased with an increasing number of action potentials in the initial discharge. Blocking the Ca-activated K conductance, by injecting EGTA [ethylene glycol-bis(.beta.-aminoethyl ether)N,N,N,N''-tetraacetic acid] into the cell, by bathing the cell in Cd, a Ca channel blocker, or by bathing the cell in Ca-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 Ca-activated K 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 Cd or of Ca-free medium. This was presumably because the Ca-activated K conductance was more developed later in the train. Accommodation was not completely abolished in the absence of Ca and presence of Cd, suggesting that other factors, in addition to Ca-activated K 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. Accommodation of the action potential discharge of hippocampal pyramidal cells may be regulated by at least 2 K currents: the Ca-activated K current and the M-current. Both of these currents are turned on during excitation of the neuron and act in an inhibitory manner on that neuron to limit further action potential discharge.