A型钾电流的增益控制：IA作为分裂抑制和消减抑制之间的开关
Gain control with A-type potassium current: IA as a switch between divisive and subtractive inhibition
摘要：
神经元处理信息的方式是将大量突触输入转化为尖峰活动。突触抑制抑制神经元的输出激发活动，并且通常被分类为对神经元的输出激发活动具有消减或分裂效应。减法抑制可以通过消除对非偏好输入的反应来缩小引起尖峰活动的输入范围。分裂性抑制是增益控制的一种形式：它在保持引起放电活动的输入范围的同时，改变放电频率。由于这两种“模式”的抑制有不同的影响神经编码，重要的是要了解的生物物理机制，区分这些反应的档案。我们使用神经元模型的模拟和数学分析，以找到抑制性输入具有减法或分裂效应的特定条件。我们确定了A型钾电流（IA）的新作用。在我们的模型中，这种快速激活、缓慢失活的外向电流充当了消减抑制和分裂抑制之间的开关。如果IA是强的（大的最大电导）和快速的（激活的时间尺度类似于尖峰启动），那么抑制对神经放电有消减作用。相反，如果IA是弱或不够快激活，那么抑制有分裂的影响神经放电。我们解释这些发现使用动力系统的方法来定义如何尖峰阈值条件依赖于突触输入和IA。我们的研究结果表明，神经元可以通过突触可塑性和/或A型钾通道的电导和动力学的调节的组合“自我调节”抑制的增益控制效应。IA的这种新作用将增加神经元和网络的灵活性，并可能与最近观察到的孤束核神经元的分裂抑制作用有关。
英文摘要：
Neurons process information by transforming barrages of synaptic inputs into spiking activity. Synaptic inhibition suppresses the output firing activity of a neuron, and is commonly classified as having a subtractive or divisive effect on a neuron's output firing activity. Subtractive inhibition can narrow the range of inputs that evoke spiking activity by eliminating responses to non-preferred inputs. Divisive inhibition is a form of gain control: it modifies firing rates while preserving the range of inputs that evoke firing activity. Since these two "modes" of inhibition have distinct impacts on neural coding, it is important to understand the biophysical mechanisms that distinguish these response profiles. We use simulations and mathematical analysis of a neuron model to find the specific conditions for which inhibitory inputs have subtractive or divisive effects. We identify a novel role for the A-type Potassium current (IA). In our model, this fast-activating, slowly- inactivating outward current acts as a switch between subtractive and divisive inhibition. If IA is strong (large maximal conductance) and fast (activates on a time-scale similar to spike initiation), then inhibition has a subtractive effect on neural firing. In contrast, if IA is weak or insufficiently fast-activating, then inhibition has a divisive effect on neural firing. We explain these findings using dynamical systems methods to define how a spike threshold condition depends on synaptic inputs and IA. Our findings suggest that neurons can "self-regulate" the gain control effects of inhibition via combinations of synaptic plasticity and/or modulation of the conductance and kinetics of A-type Potassium channels. This novel role for IA would add flexibility to neurons and networks, and may relate to recent observations of divisive inhibitory effects on neurons in the nucleus of the solitary tract.
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