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活动依赖性细胞外钙离子和钾离子变化揭示了脊髓运动相关网络中的起搏器。

Activity-dependent changes in extracellular Ca2+ and K+ reveal pacemakers in the spinal locomotor-related network.

机构信息

Team P3M, Institut de Neurosciences de la Timone, UMR 7289, CNRS and Aix-Marseille Université, F-13385 Marseille, France.

出版信息

Neuron. 2013 Mar 20;77(6):1047-54. doi: 10.1016/j.neuron.2013.01.026.

DOI:10.1016/j.neuron.2013.01.026
PMID:23522041
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3736142/
Abstract

Changes in the extracellular ionic concentrations occur as a natural consequence of firing activity in large populations of neurons. The extent to which these changes alter the properties of individual neurons and the operation of neuronal networks remains unknown. Here, we show that the locomotor-like activity in the isolated neonatal rodent spinal cord reduces the extracellular calcium ([Ca(2+)]o) to 0.9 mM and increases the extracellular potassium ([K(+)]o) to 6 mM. Such changes in [Ca(2+)]o and [K(+)]o trigger pacemaker activities in interneurons considered to be part of the locomotor network. Experimental data and a modeling study show that the emergence of pacemaker properties critically involves a [Ca(2+)]o-dependent activation of the persistent sodium current (INaP). These results support a concept for locomotor rhythm generation in which INaP-dependent pacemaker properties in spinal interneurons are switched on and tuned by activity-dependent changes in [Ca(2+)]o and [K(+)]o.

摘要

细胞外离子浓度的变化是神经元群体放电活动的自然结果。这些变化在多大程度上改变单个神经元的特性和神经元网络的运作尚不清楚。在这里,我们表明,分离的新生啮齿动物脊髓中的类似运动的活动将细胞外钙([Ca(2+)]o)降低至 0.9 mM,并将细胞外钾([K(+)]o)增加至 6 mM。[Ca(2+)]o 和 [K(+)]o 的这种变化会引发被认为是运动网络一部分的中间神经元的起搏器活动。实验数据和建模研究表明,起搏器特性的出现关键涉及到依赖于[Ca(2+)]o 的持续钠电流(INaP)的激活。这些结果支持了一种运动节律产生的概念,其中脊髓中间神经元中依赖于 INaP 的起搏器特性通过[Ca(2+)]o 和 [K(+)]o 的活动依赖性变化而被开启和调整。

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Identification of minimal neuronal networks involved in flexor-extensor alternation in the mammalian spinal cord.鉴定参与哺乳动物脊髓屈伸交替的最小神经元网络。
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Specific brainstem neurons switch each other into pacemaker mode to drive movement by activating NMDA receptors.
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bioRxiv. 2025 May 22:2025.05.17.654682. doi: 10.1101/2025.05.17.654682.
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