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Unique features of action potential initiation in cortical neurons.

机译：皮质神经元动作电位启动的独特特征。

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摘要

Neurons process and encode information by generating sequences of action potentials. For all spiking neurons, the encoding of single-neuron computations into sequences of spikes is biophysically determined by the cell's action-potential-generating mechanism. It has recently been discovered that apparently minor modifications of this mechanism can qualitatively change the nature of neuronal encoding. Here we quantitatively analyse the dynamics of action potential initiation in cortical neurons in vivo, in vitro and in computational models. Unexpectedly, key features of the initiation dynamics of cortical neuron action potentials--their rapid initiation and variable onset potential--are outside the range of behaviours described by the classical Hodgkin-Huxley theory. We propose a new model based on the cooperative activation of sodium channels that reproduces the observed dynamics of action potential initiation. This new model predicts that Hodgkin-Huxley-type dynamics of action potential initiation can be induced by artificially decreasing the effective density of sodium channels. In vitro experiments confirm this prediction, supporting the hypothesis that cooperative sodium channel activation underlies the dynamics of action potential initiation in cortical neurons.
机译：神经元通过产生动作电位序列来处理和编码信息。对于所有加标的神经元，单神经元计算到尖峰序列中的编码是通过细胞的动作电位生成机制进行生物学上的确定的。最近发现，该机制的明显修饰可以定性地改变神经元编码的性质。在这里，我们定量分析了体内，体外和计算模型中皮层神经元中动作电位启动的动力学。出乎意料的是，皮层神经元动作电位的起始动力学的关键特征-它们的快速起始和可变的发作电位-超出了经典霍奇金-赫克斯利理论描述的行为范围。我们提出了一个基于钠通道协同激活的新模型，该模型可再现观察到的动作电位引发的动力学。该新模型预测，可以通过人为降低钠通道的有效密度来诱导霍奇金-赫克斯利型动作电位的动力学。体外实验证实了这一预测，支持了以下假设：协同钠通道激活是皮层神经元中动作电位启动动力学的基础。

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