Yoo Seung-Wan, Motari Mary G, Schnaar Ronald L
Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, 21205.
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, 21205.
J Comp Neurol. 2017 Feb 1;525(2):291-301. doi: 10.1002/cne.24064. Epub 2016 Jul 8.
The corpus callosum (CC) is the largest fiber tract in the mammalian brain, linking the bilateral cerebral hemispheres. CC development depends on the proper balance of axon growth cone attractive and repellent cues leading axons to the midline and then directing them to the contralateral hemisphere. Imbalance of these cues results in CC agenesis or dysgenesis. Nogo receptors (NgR1, NgR2, and NgR3) are growth cone directive molecules known for inhibiting axon regeneration after injury. We report that mice lacking Nogo receptors (NgR123-null mice) display complete CC agenesis due to axon misdirection evidenced by ectopic axons including cortical Probst bundles. Because glia and glial-derived growth cone repellent factors (especially the diffusible factor Slit2) are required for CC development, their distribution was studied. Compared with wild-type mice, NgR123-null mice had a sharp increase in the glial marker glial fibrillary acidic protein (GFAP) and in Slit2 at the glial wedge and indusium griseum, midline structures required for CC formation. NgR123-null mice displayed reduced motor coordination and hyperactivity. These data are consistent with the hypotheses that Nogo receptors are membrane-bound growth cone repellent factors required for migration of axons across the midline at the CC, and that their absence results directly or indirectly in midline gliosis, increased Slit2, and complete CC agenesis. J. Comp. Neurol. 525:291-301, 2017. © 2016 Wiley Periodicals, Inc.
胼胝体(CC)是哺乳动物大脑中最大的纤维束,连接双侧大脑半球。CC的发育取决于轴突生长锥吸引和排斥信号的适当平衡,这些信号引导轴突到达中线,然后将它们导向对侧半球。这些信号的失衡会导致CC发育不全或发育异常。Nogo受体(NgR1、NgR2和NgR3)是生长锥导向分子,以抑制损伤后的轴突再生而闻名。我们报告,缺乏Nogo受体的小鼠(NgR123基因敲除小鼠)表现出完全的CC发育不全,这是由于轴突误向导致的,异位轴突包括皮质普罗布斯特束可证明这一点。由于胶质细胞和胶质细胞衍生的生长锥排斥因子(尤其是可扩散因子Slit2)是CC发育所必需的,因此研究了它们的分布。与野生型小鼠相比,NgR123基因敲除小鼠在胶质楔和灰被(CC形成所需的中线结构)处的胶质细胞标志物胶质纤维酸性蛋白(GFAP)和Slit2急剧增加。NgR123基因敲除小鼠表现出运动协调性降低和多动。这些数据与以下假设一致:Nogo受体是轴突在CC处跨越中线迁移所需的膜结合生长锥排斥因子,其缺失直接或间接导致中线胶质增生、Slit2增加和完全的CC发育不全。《比较神经学杂志》525:291 - 301,2017年。©2016威利期刊公司。