Myelin associated inhibitors: A link between injury-induced and experience-dependent plasticity

被引:114
作者
Akbik, Feras
Cafferty, William B. J.
Strittmatter, Stephen M. [1 ]
机构
[1] Yale Univ, Sch Med, Program Cellular Neurosci Neurodegenerat & Repair, New Haven, CT 06536 USA
基金
美国国家卫生研究院;
关键词
Spinal cord injury; Axons; Plasticity; Regeneration; Experience-dependent plasticity; Activity dependent plasticity; Nogo; Nogo-Receptor-1; MAG; OMgp; PirB; Stroke; Myelin; SPINAL-CORD-INJURY; NEURITE GROWTH-INHIBITORS; CENTRAL-NERVOUS-SYSTEM; OCULAR-DOMINANCE PLASTICITY; MONOCLONAL-ANTIBODY IN-1; RECEPTOR FAMILY-MEMBER; ADULT VISUAL-CORTEX; NOGO MESSENGER-RNA; AXONAL REGENERATION; FUNCTIONAL RECOVERY;
D O I
10.1016/j.expneurol.2011.06.006
中图分类号
Q189 [神经科学];
学科分类号
071006 [神经生物学];
摘要
In the adult, both neurologic recovery and anatomical growth after a CNS injury are limited. Two classes of growth inhibitors, myelin associated inhibitors (MAIs) and extracellular matrix associated inhibitors, limit both functional recovery and anatomical rearrangements in animal models of spinal cord injury. Here we focus on how MAIs limit a wide spectrum of growth that includes regeneration, sprouting, and plasticity in both the intact and lesioned CNS. Three classic myelin associated inhibitors, Nogo-A. MAG, and OMgp, signal through their common receptors, Nogo-66 Receptor-1 (NgR1) and Paired-Immunoglobulin-like-Receptor-B (PirB), to regulate cytoskeletal dynamics and inhibit growth. Initially described as inhibitors of axonal regeneration, subsequent work has demonstrated that MAIs also limit activity and experience-dependent plasticity in the intact, adult CNS. MAls therefore represent a point of convergence for plasticity that limits anatomical rearrangements regardless of the inciting stimulus, blurring the distinction between injury studies and more "basic" plasticity studies. (C) 2011 Elsevier Inc. All rights reserved.
引用
收藏
页码:43 / 52
页数:10
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