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追溯你的足迹:损伤后脊髓网络可塑性的发育见解

Retracing your footsteps: developmental insights to spinal network plasticity following injury.

作者信息

Jean-Xavier C, Sharples S A, Mayr K A, Lognon A P, Whelan P J

机构信息

Hotchkiss Brain Institute, University of Calgary , Calgary, Alberta , Canada.

Department of Comparative Biology and Experimental Medicine, University of Calgary , Calgary, Alberta , Canada.

出版信息

J Neurophysiol. 2018 Feb 1;119(2):521-536. doi: 10.1152/jn.00575.2017. Epub 2017 Oct 25.

Abstract

During development of the spinal cord, a precise interaction occurs between descending projections and sensory afferents, with spinal networks that lead to expression of coordinated motor output. In the rodent, during the last embryonic week, motor output first occurs as regular bursts of spontaneous activity, progressing to stochastic patterns of episodes that express bouts of coordinated rhythmic activity perinatally. Locomotor activity becomes functionally mature in the 2nd postnatal wk and is heralded by the onset of weight-bearing locomotion on the 8th and 9th postnatal day. Concomitantly, there is a maturation of intrinsic properties and key conductances mediating plateau potentials. In this review, we discuss spinal neuronal excitability, descending modulation, and afferent modulation in the developing rodent spinal cord. In the adult, plastic mechanisms are much more constrained but become more permissive following neurotrauma, such as spinal cord injury. We discuss parallel mechanisms that contribute to maturation of network function during development to mechanisms of pathological plasticity that contribute to aberrant motor patterns, such as spasticity and clonus, which emerge following central injury.

摘要

在脊髓发育过程中,下行投射与感觉传入之间会发生精确的相互作用,进而形成导致协调运动输出表达的脊髓网络。在啮齿动物中,在胚胎期的最后一周,运动输出首先以规则的自发活动爆发形式出现,随后发展为随机的发作模式,在围产期表现为一阵阵协调的节律性活动。运动活动在出生后第2周功能成熟,并在出生后第8天和第9天开始负重运动时表现出来。与此同时,介导平台电位的内在特性和关键电导也会成熟。在这篇综述中,我们讨论了发育中的啮齿动物脊髓中的脊髓神经元兴奋性、下行调制和传入调制。在成体中,可塑性机制受到更多限制,但在诸如脊髓损伤等神经创伤后会变得更加宽松。我们讨论了在发育过程中有助于网络功能成熟的平行机制,以及导致异常运动模式(如中枢损伤后出现的痉挛和阵挛)的病理性可塑性机制。

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