Naundorf Björn, Wolf Fred, Volgushev Maxim
Max Planck Institute for Dynamics and Self-Organization, University of Göttingen, Bunsenstr. 10, D-37073 Göttingen, Germany.
Nature. 2006 Apr 20;440(7087):1060-3. doi: 10.1038/nature04610.
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.
神经元通过产生动作电位序列来处理和编码信息。对于所有的脉冲神经元来说，将单神经元计算编码为脉冲序列在生物物理学上是由细胞的动作电位产生机制决定的。最近发现，该机制看似微小的改变可能会在性质上改变神经元编码的本质。在这里，我们定量分析了体内、体外皮质神经元以及计算模型中动作电位起始的动力学。出乎意料的是，皮质神经元动作电位起始动力学的关键特征——它们的快速起始和可变的起始电位——超出了经典霍奇金-赫胥黎理论所描述的行为范围。我们提出了一个基于钠通道协同激活的新模型，该模型再现了观察到的动作电位起始动力学。这个新模型预测，通过人为降低钠通道的有效密度，可以诱导出霍奇金-赫胥黎型的动作电位起始动力学。体外实验证实了这一预测，支持了协同钠通道激活是皮质神经元动作电位起始动力学基础的假说。
