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Ca(v)1.2 calcium channels modulate the spiking pattern of hippocampal pyramidal cells

机译：Ca（v）1.2钙通道调节海马锥体细胞的突触模式

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摘要

Ca(v)1.2 L-type calcium channels support hippocampal synaptic plasticity, likely by facilitating dendritic Ca2+ influx evoked by action potentials (AP) back-propagated from the soma. Ca2+ influx into hippocampal neurons during somatic AN is sufficient to activate signalling pathways associated with late phase LTP. Thus, mechanisms controlling AP firing of hippocampal neurons are of major functional relevance. We examined the excitability of CA1 pyramidal cells using somatic current-clamp recordings in brain slices from control type mice and mice with the Ca(v)1.2 gene inactivated in principal hippocampal neurons. Lack of the Ca(v)1.2 protein did not affect either affect basic characteristics, such as resting membrane potential and input resistance, or parameters of single action potentials (AP) induced by 5 ms depolarising current pulses. However, CA1 hippocampal neurons from control and mutant mice differed in their patterns of AP firing during 500 ms depolarising current pulses: threshold voltage for repetitive firing was shifted significantly by about 5 mV to more depolarised potentials in the mutant mice (p<0.01), and the latency until firing of the first AP was prolonged (73.2 +/- 6.6 ms versus 48.1 +/- 7.8 ms in control; p < 0.05). CA1 pyramidal cells from the mutant mice also showed a lowered initial spiking frequency within an AP train. In control cells, isradipine had matching effects, while BayK 8644 facilitated spiking. Our data demonstrate that Ca(v)1.2 channels are involved in regulating the intrinsic excitability of CA1 pyramidal neurons. This cellular mechanism may contribute to the known function of Ca(v)1.2 channels in supporting synaptic plasticity and memory. (C) 2007 Elsevier Inc. All rights reserved.
机译：Ca（v）1.2 L型钙通道支持海马突触可塑性，可能是通过促进从体细胞向后传播的动作电位（AP）诱发的树突状Ca2 +内流。体细胞AN期间Ca2 +流入海马神经元足以激活与晚期LTP相关的信号通路。因此，控制海马神经元AP放电的机制具有主要的功能相关性。我们检查了CA1锥体细胞的兴奋性，使用来自控制型小鼠和在主要海马神经元中失活的Ca（v）1.2基因的小鼠的脑切片中的体电流钳记录。缺少Ca（v）1.2蛋白不会影响基本特性，例如静息膜电位和输入电阻，也不会影响5 ms去极化电流脉冲引起的单动电位（AP）参数。但是，来自对照小鼠和突变小鼠的CA1海马神经元在500毫秒去极化电流脉冲期间的AP放电模式有所不同：重复激发的阈值电压显着移动了约5 mV，从而使突变小鼠的去极化电位更高（p <0.01），并延长了第一个AP发射的等待时间（对照组为73.2 +/- 6.6毫秒，而对照组为48.1 +/- 7.8毫秒; p <0.05）。来自突变小鼠的CA1锥体细胞在AP训练中还显示出较低的初始加标频率。在对照细胞中，伊拉地平具有匹配作用，而BayK 8644则促进了加标作用。我们的数据表明，Ca（v）1.2通道参与调节CA1锥体神经元的内在兴奋性。此细胞机制可能有助于Ca（v）1.2通道在支持突触可塑性和记忆中的已知功能。 （C）2007 Elsevier Inc.保留所有权利。

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