Contribution of persistent Na+ current and M-type K+ current to somatic bursting in CA1 pyramidal cells:: Combined experimental and modeling study
Contribution of persistent Na+ current and M-type K+ current to somatic bursting in CA1 pyramidal cells:: Combined experimental and modeling study
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DOI：
10.1152/jn.00205.2006
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发表时间：
2006-10-01
影响因子：
2.5
通讯作者：
Yaari, Yoel
中科院分区：
文献类型：
--
作者：
Golomb, David;Yue, Cuiyong;Yaari, Yoel
持续Na+电流和m型K+电流对CA1锥体细胞体细胞破裂的贡献：实验与模型相结合的研究。[J]中国生物医学工程学报（英文版），2006。首次出版于2006年6月28日；doi: 10.1152 /约。00205.2006. 成年CA1锥体细胞的固有放电模式根据细胞外环境的离子组成，沿着从规则放电到节律性爆发的连续“爆发”变化。暴露于正常细胞外Ca2+浓度（[Ca2+](o)）的神经元突发性低，但通过降低[Ca2+](o)而显着增强，尽管不是通过阻断Ca2+和Ca2+激活的K+电流。我们使用细胞内记录显示，即使在截断顶端树突后，低[Ca2+](o)的爆发仍然存在，这表明爆发是由体细胞或体细胞附近的膜电流相互作用产生的。为了研究破裂的机制，我们构建了一个基于电导的CA1锥体神经元单室模型。在这个神经元模型中，最近的实验结果表明，通过负移动持续Na+电流（I-NaP）的激活曲线来模拟[Ca2+](o)的减少。神经元模型解释了不同的参数集，在零和正常[Ca2+](o)下实验观察到的放电模式的多样性。在神经元模型中，增加INaP可以诱导爆发，并增加爆发内的峰值数量，但这既不是爆发的必要条件，也不是爆发的充分条件。我们使用快慢分析和分岔理论表明，如果产生尖峰电流的动力学足够快（尽管不是非常快），则m型K+电流（I-M）可以通过在安静状态和张力活跃状态之间转换神经元行为来实现破裂。我们认为CA1锥体细胞的破裂可以用单室“方形破裂”机制来解释，其中有一个缓慢的变量，即I-M的激活。
Contribution of persistent Na+ current and M-type K+ current to somatic bursting in CA1 pyramidal cells: combined experimental and modeling Study. J Neurophysiol 96: 1912-1926, 2006. First published June 28, 2006; doi: 10.1152/jn. 00205.2006. The intrinsic firing modes of adult CA1 pyramidal cells vary along a continuum of "burstiness" from regular firing to rhythmic bursting, depending on the ionic composition of the extracellular milieu. Burstiness is low in neurons exposed to a normal extracellular Ca2+ concentration ([Ca2+](o)), but is markedly enhanced by lowering [Ca2+](o), although not by blocking Ca2+ and Ca2+-activated K+ currents. We show, using intracellular recordings, that burstiness in low [Ca2+](o) persists even after truncating the apical dendrites, suggesting that bursts are generated by an interplay of membrane currents at or near the soma. To study the mechanisms of bursting, we have constructed a conductance-based, one-compartment model of CA1 pyramidal neurons. In this neuron model, reduced [Ca2+](o) is simulated by negatively shifting the activation curve of the persistent Na+ current (I-NaP) as indicated by recent experimental results. The neuron model accounts, with different parameter sets, for the diversity of firing patterns observed experimentally in both zero and normal [Ca2+](o). Increasing INaP in the neuron model induces bursting and increases the number of spikes within a burst but is neither necessary nor sufficient for bursting. We show, using fast-slow analysis and bifurcation theory, that the M-type K+ current (I-M) allows bursting by shifting neuronal behavior between a silent and a tonically active state provided the kinetics of the spike generating currents are sufficiently, although not extremely, fast. We suggest that bursting in CA1 pyramidal cells can be explained by a single compartment "square bursting" mechanism with one slow variable, the activation of I-M.