Patel Ameera X, Burdakov Denis
Brain Mapping Unit, University of Cambridge, Cambridge, UK.
MRC National Institute for Medical Research, London, UK; MRC Centre for Developmental Neurobiology, King's College London, London, UK.
PLoS One. 2015 Mar 27;10(3):e0115431. doi: 10.1371/journal.pone.0115431. eCollection 2015.
Gain modulation is a key feature of neural information processing, but underlying mechanisms remain unclear. In single neurons, gain can be measured as the slope of the current-frequency (input-output) relationship over any given range of inputs. While much work has focused on the control of basal firing rates and spike rate adaptation, gain control has been relatively unstudied. Of the limited studies on gain control, some have examined the roles of synaptic noise and passive somatic currents, but the roles of voltage-gated channels present ubiquitously in neurons have been less explored. Here, we systematically examined the relationship between gain and voltage-gated ion channels in a conductance-based, tonically-active, model neuron. Changes in expression (conductance density) of voltage-gated channels increased (Ca2+ channel), reduced (K+ channels), or produced little effect (h-type channel) on gain. We found that the gain-controlling ability of channels increased exponentially with the steepness of their activation within the dynamic voltage window (voltage range associated with firing). For depolarization-activated channels, this produced a greater channel current per action potential at higher firing rates. This allowed these channels to modulate gain by contributing to firing preferentially at states of higher excitation. A finer analysis of the current-voltage relationship during tonic firing identified narrow voltage windows at which the gain-modulating channels exerted their effects. As a proof of concept, we show that h-type channels can be tuned to modulate gain by changing the steepness of their activation within the dynamic voltage window. These results show how the impact of an ion channel on gain can be predicted from the relationship between channel kinetics and the membrane potential during firing. This is potentially relevant to understanding input-output scaling in a wide class of neurons found throughout the brain and other nervous systems.
增益调制是神经信息处理的一个关键特征,但其潜在机制仍不清楚。在单个神经元中,增益可以通过在任何给定输入范围内的电流-频率(输入-输出)关系的斜率来测量。虽然许多研究都集中在对基础放电率和放电率适应性的控制上,但增益控制相对较少被研究。在关于增益控制的有限研究中,一些研究考察了突触噪声和被动体细胞电流的作用,但神经元中普遍存在的电压门控通道的作用则较少被探索。在这里,我们在一个基于电导、持续活动的模型神经元中系统地研究了增益与电压门控离子通道之间的关系。电压门控通道表达(电导密度)的变化对增益产生了增加(钙通道)、降低(钾通道)或几乎没有影响(h型通道)的效果。我们发现,通道的增益控制能力随着其在动态电压窗口(与放电相关的电压范围)内激活的陡峭程度呈指数增加。对于去极化激活通道,这使得在较高放电率时每个动作电位产生更大的通道电流。这使得这些通道能够通过在更高兴奋状态下优先促进放电来调节增益。对持续放电期间电流-电压关系的更精细分析确定了增益调制通道发挥作用的狭窄电压窗口。作为概念验证,我们表明h型通道可以通过改变其在动态电压窗口内激活的陡峭程度来调节增益。这些结果表明了如何从通道动力学与放电期间膜电位之间的关系预测离子通道对增益的影响。这可能与理解遍布大脑和其他神经系统的广泛神经元类别的输入-输出缩放有关。