Division of Biology and Bioengineering, California Institute of Technology Pasadena, CA, USA ; Allen Institute for Brain Science Seattle, WA, USA.
Allen Institute for Brain Science Seattle, WA, USA.
Front Comput Neurosci. 2014 Aug 14;8:89. doi: 10.3389/fncom.2014.00089. eCollection 2014.
Apical and tuft dendrites of pyramidal neurons support regenerative electrical potentials, giving rise to long-lasting (approximately hundreds of milliseconds) and strong (~50 mV from rest) depolarizations. Such plateau events rely on clustered glutamatergic input, can be mediated by calcium or by NMDA currents, and often generate somatic depolarizations that last for the time course of the dendritic plateau event. We address the computational significance of such single-neuron processing via reduced but biophysically realistic modeling. We introduce a model based on two discrete integration zones, a somatic and a dendritic one, that communicate from the dendritic to the somatic compartment via a long plateau-conductance. We show principled differences in the way dendritic vs. somatic inhibition controls spike timing, and demonstrate how this could implement spike time control in the face of barrages of synaptic inputs.
树突棘和树突的顶端支持再生性的电潜能,从而产生持久的(大约数百毫秒)和强烈的(相对于静息电位的~50 mV)去极化。这种平台事件依赖于聚集的谷氨酸能输入,可以通过钙电流或 NMDA 电流介导,并且通常产生持续时间与树突平台事件相当的体部去极化。我们通过简化但具有生理现实性的建模来研究这种单个神经元处理的计算意义。我们引入了一个基于两个离散积分区的模型,一个是体部的,一个是树突的,通过长的平台电导从树突向体部腔室进行通讯。我们展示了树突与体部抑制控制尖峰时间的方式的原则性差异,并演示了如何在面对突触输入的弹幕时实现尖峰时间控制。