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Spikelets in Pyramidal Neurons: Action Potentials Initiated in the Axon Initial Segment That Do Not Activate the Soma

机译:锥体神经元中的小穗:轴突初始段中启动的动作电位不会激活躯体

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摘要

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.
机译:小穗为小穗状去极化,可在体细胞内记录中测量。它们起源于锥体神经元仍有争议。为了解释小穗的产生,我们提出了一种新颖的单细胞机制:体细胞树突状输入在轴突起始段产生动作电位,可能无法激活体细胞并表现为体细胞小穗。通过对间隔神经元模型的数学分析和数值模拟,我们确定了控制小尖峰生成的四个关键因素:(1)发射阈值的差异,(2)阻抗不匹配以及(3)躯体和轴突初始段之间的电声分离,分别为以及(4)输入幅度。因为小穗会沿着轴突向前传播动作电位,而它们却避免了体-树突状区室的完全去极化,因此我们推测,这种操作模式可以节省能量并调节树突状可塑性,同时仍然允许读出神经元计算的结果。

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