Michalikova Martina, Remme Michiel W H, Kempter Richard
Institute for Theoretical Biology, Department of Biology, Humboldt-Universität zu Berlin, Berlin, Germany.
Bernstein Center for Computational Neuroscience Berlin, Berlin, Germany.
PLoS Comput Biol. 2017 Jan 9;13(1):e1005237. doi: 10.1371/journal.pcbi.1005237. eCollection 2017 Jan.
Spikelets are small spike-like depolarizations that can be measured in somatic intracellular recordings. Their origin in pyramidal neurons remains controversial. To explain spikelet generation, we propose a novel single-cell mechanism: somato-dendritic input generates action potentials at the axon initial segment that may fail to activate the soma and manifest as somatic spikelets. Using mathematical analysis and numerical simulations of compartmental neuron models, we identified four key factors controlling spikelet generation: (1) difference in firing threshold, (2) impedance mismatch, and (3) electrotonic separation between the soma and the axon initial segment, as well as (4) input amplitude. Because spikelets involve forward propagation of action potentials along the axon while they avoid full depolarization of the somato-dendritic compartments, we conjecture that this mode of operation saves energy and regulates dendritic plasticity while still allowing for a read-out of results of neuronal computations.
小棘波是在体细胞内记录中可以测量到的小的尖峰状去极化。它们在锥体神经元中的起源仍存在争议。为了解释小棘波的产生，我们提出了一种新的单细胞机制：体-树突输入在轴突起始段产生动作电位，这些动作电位可能无法激活胞体，并表现为体细胞小棘波。通过对神经元模型的数学分析和数值模拟，我们确定了控制小棘波产生的四个关键因素：（1）放电阈值差异，（2）阻抗失配，（3）胞体与轴突起始段之间的电紧张分离，以及（4）输入幅度。由于小棘波涉及动作电位沿轴突的正向传播，同时避免体-树突区室的完全去极化，我们推测这种操作模式在节省能量和调节树突可塑性的同时，仍能读出神经元计算的结果。
