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首页> 外文期刊>Journal of Neurophysiology >A computational model for how the fast afterhyperpolarization paradoxically increases gain in regularly firing neurons
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A computational model for how the fast afterhyperpolarization paradoxically increases gain in regularly firing neurons

机译：如何快速后经过矛盾的矛盾的计算模型增加了常规发射神经元的增益

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摘要

The gain of a neuron, the number and frequency of action potentials triggered in response to a given amount of depolarizing injection, is an important behavior underlying a neuron's function. Variations in action potential waveform can influence neuronal discharges by the differential activation of voltage-and ion-gated channels long after the end of a spike. One component of the action potential waveform, the afterhyperpolarization (AHP), is generally considered an inhibitory mechanism for limiting firing rates. In dentate gyrus granule cells (DGCs) expressing fast-gated BK channels, large fast AHPs (fAHP) are paradoxically associated with increased gain. In this article, we describe a mechanism for this behavior using a computational model. Hyperpolarization provided by the fAHP enhances activation of a dendritic inward current (a T-type Ca2+ channel is suggested) that, in turn, boosts rebound depolarization at the soma. The model suggests that the fAHP may both reduce Ca2+ channel inactivation and, counterintuitively, enhance its activation. The magnitude of the rebound depolarization, in turn, determines the activation of a subsequent, slower inward current (a persistent Na+ current is suggested) limiting the interspike interval. Simulations also show that the effect of AHP on gain is also effective for physiologically relevant stimulation; varying AHP amplitude affects interspike interval across a range of "noisy" stimulus frequency and amplitudes. The mechanism proposed suggests that small fAHPs in DGCs may contribute to their limited excitability.
机译：神经元的增益，响应于给定量的去极化注射率触发的动作电位的数量和频率是神经元功能的重要行为。动作电位波形的变化可以通过电压和离子门控通道的差动激活来影响神经元放电，在钉极端之后长。动作电位波形的一个组分，后胚性（AHP）通常被认为是限制烧制率的抑制机制。在表达快速门控BK通道的牙齿颗粒细胞（DGCS）中，大的快速AHPS（FAHP）与增加的增益矛盾相关。在本文中，我们描述了使用计算模型的这种行为的机制。由FAHP提供的超极化增强了树枝状内向电流的激活（建议T型CA2 +通道），反过来又提高了SOMA的反弹去极化。该模型表明，FAHP可以降低CA2 +信道失活，并违反直接增强其激活。反弹去极化的大小反过来决定了随后的激活，较慢的向内电流（建议持久Na +电流）限制间隔间隔。仿真还表明，AHP对生理相关刺激的增益的影响也有效;变化的AHP振幅会影响一系列“嘈杂”刺激频率和幅度的间隙间隔。提出的机制表明，DGCS中的小型FAHP可能有助于其有限的兴奋性。

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