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持续性内向电流对运动神经元突触抑制的多种放大模式。

Multiple modes of amplification of synaptic inhibition to motoneurons by persistent inward currents.

作者信息

Bui Tuan V, Grande Giovanbattista, Rose P Ken

机构信息

Canadian Institutes of Health Research Group in Sensory-Motor Systems, Department of Physiology, Centre for Neuroscience Studies, Queen's University, Kingston, Canada.

出版信息

J Neurophysiol. 2008 Feb;99(2):571-82. doi: 10.1152/jn.00717.2007. Epub 2007 Nov 28.

DOI:10.1152/jn.00717.2007
PMID:18046007
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2930909/
Abstract

The ability of inhibitory synaptic inputs to dampen the excitability of motoneurons is augmented when persistent inward currents (PICs) are activated. This amplification could be due to an increase in the driving potential of inhibitory synapses or the deactivation of the channels underlying PICs. Our goal was to determine which mechanism leads to the amplification of inhibitory inputs by PICs. To reach this goal, we measured inhibitory postsynaptic currents (IPSCs) in decerebrate cats during somatic voltage-clamp steps. These IPSCs were generated by tonic activation of Renshaw cells. The IPSCs exhibited a rapid rise and a slower decay to a plateau level. Activation of PICs always led to an increase in the peak of the IPSC, but the amount of decay after the peak of the IPSC was inversely related to the size of the IPSC. These results were replicated in simulations based on compartmental models of motoneurons incorporating distributions of Renshaw cell synapses based on anatomical observations, and L-type calcium channels distributed as 100-microm-long hot spots centered 100 to 400 microm away from the soma. For smaller IPSCs, amplification by PICs was due to an increase in the driving force of the inhibitory synaptic current. For larger IPSCs, amplification was caused by deactivation of the channels underlying PICs leading to a lesser decay of the IPSCs. As a result of this change in the time course of the IPSC, deactivation of the channels underlying PICs leads to a greater amplification of the total inhibitory synaptic current.

摘要

当持续性内向电流(PICs)被激活时,抑制性突触输入减弱运动神经元兴奋性的能力会增强。这种放大可能是由于抑制性突触驱动电位的增加或PICs相关通道的失活。我们的目标是确定哪种机制导致PICs对抑制性输入的放大作用。为了实现这一目标,我们在去大脑猫的躯体电压钳制步骤中测量了抑制性突触后电流(IPSCs)。这些IPSCs由闰绍细胞的强直性激活产生。IPSCs表现出快速上升和较慢衰减至平台期水平。PICs的激活总是导致IPSC峰值增加,但IPSC峰值后的衰减量与IPSC大小呈负相关。基于运动神经元的房室模型进行的模拟复制了这些结果,该模型结合了基于解剖学观察的闰绍细胞突触分布,以及以距离胞体100至400微米为中心、长度为100微米的热点分布的L型钙通道。对于较小的IPSCs而言,PICs的放大作用是由于抑制性突触电流驱动力的增加。对于较大的IPSCs,放大作用是由PICs相关通道的失活导致IPSCs衰减较小引起的。由于IPSC时间过程的这种变化,PICs相关通道的失活导致总抑制性突触电流有更大的放大。

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