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分析 Nogo-A 基因敲除小鼠视神经交叉处的轴突分支。

Analysis of axon divergence at the optic chiasm in nogo-a knockout mice.

机构信息

Department of Neurology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong, China; Medical Examination Center, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong, China.

Department of Neurology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong, China.

出版信息

Neurosci Lett. 2020 Jul 13;731:135109. doi: 10.1016/j.neulet.2020.135109. Epub 2020 May 31.

DOI:10.1016/j.neulet.2020.135109
PMID:32492476
Abstract

Our earlier studies have shown that the axon growth inhibitory molecule Nogo affects axon routing at the optic chiasm likely through a differential regulation of Nogo receptor on the optic axons. Using isoform specific antibodies, we further showed that Nogo-A was predominantly expressed by retinal ganglion cells and their axons, while Nogo-B was highly localized on the radial glia at the midline of the chiasm, suggesting a role of Nogo-B in regulating turning of uncrossed axons. To further investigate the roles of Nogo-A in axon divergence, we analyzed the routing of axons in the chiasm of Nogo-A knockout mice during the growth of axons across the midline. At E13 to E16, there was no significant difference in the contralateral projection (P = 0.6943 for E13; P = 0.9867 for E14; P = 0.4121 for E15 and P = 0.3402 for E16). The results also showed the absence of Nogo-A did not cause any obvious change to the ipsilateral projection at the optic chiasm, both for the early generated uncrossed axons at E13 and E14 and the late cohorts at E15-E16, when compared with the wild-type mice (P = 0.4788 for E13; P = 0.188 for E14; P = 0.3152 for E15 and P = 0.432 for E16). These findings support that Nogo-A is not the major isoform to guide the axon divergence in the mouse optic chiasm.

摘要

我们之前的研究表明,轴突生长抑制分子 Nogo 通过对视轴突上的 Nogo 受体的差异调节来影响视交叉处的轴突路由。使用同工型特异性抗体,我们进一步表明 Nogo-A 主要由视网膜神经节细胞及其轴突表达,而 Nogo-B 则高度定位于视交叉中线的放射状胶质上,表明 Nogo-B 在调节未交叉轴突的转向中起作用。为了进一步研究 Nogo-A 在轴突发散中的作用,我们分析了 Nogo-A 敲除小鼠在视轴突穿过中线生长过程中视交叉处轴突的路由。在 E13 至 E16 期间,对侧投射没有明显差异(E13 时 P = 0.6943;E14 时 P = 0.9867;E15 时 P = 0.4121;E16 时 P = 0.3402)。结果还表明,Nogo-A 的缺失不会对视交叉处同侧投射造成任何明显变化,无论是在 E13 和 E14 时早期生成的未交叉轴突,还是在 E15-E16 时晚期生成的轴突,与野生型小鼠相比(E13 时 P = 0.4788;E14 时 P = 0.188;E15 时 P = 0.3152;E16 时 P = 0.432)。这些发现支持 Nogo-A 不是指导小鼠视交叉处轴突发散的主要同工型。

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