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Contactin1a的表达与斑马鱼中枢神经系统中少突胶质细胞的分化和轴突再生有关。

Contactin1a expression is associated with oligodendrocyte differentiation and axonal regeneration in the central nervous system of zebrafish.

作者信息

Schweitzer Jörn, Gimnopoulos Dimitrios, Lieberoth Bettina C, Pogoda Hans-Martin, Feldner Julia, Ebert Anselm, Schachner Melitta, Becker Thomas, Becker Catherina G

机构信息

Institut für die Biosynthese Neuraler Strukturen, Zentrum für Molekulare Neurobiologie, University of Hamburg, D-20246 Hamburg, Germany.

出版信息

Mol Cell Neurosci. 2007 Jun;35(2):194-207. doi: 10.1016/j.mcn.2007.02.018. Epub 2007 Mar 3.

Abstract

Contactin1a (Cntn1a) is a zebrafish homolog of contactin1 (F3/F11/contactin) in mammals, an immunoglobulin superfamily recognition molecule of neurons and oligodendrocytes. We describe conspicuous Cntn1a mRNA expression in oligodendrocytes in the developing optic pathway of zebrafish. In adults, this expression is only retained in glial cells in the intraretinal optic fiber layer, which contains 'loose' myelin. After optic nerve lesion, oligodendrocytes re-express Cntn1a mRNA independently of the presence of regenerating axons and retinal ganglion cells upregulate Cntn1a expression to levels that are significantly higher than those during development. After spinal cord lesion, expression of Cntn1a mRNA is similarly increased in axotomized brainstem neurons and white matter glial cells in the spinal cord. In addition, reduced mRNA expression in the trigeminal/anterior lateral line ganglion in erbb3-deficient mutant larvae implies Cntn1a in Schwann cell differentiation. These complex regulation patterns suggest roles for Cntn1a in myelinating cells and neurons particularly in successful CNS regeneration.

摘要

Contactin1a(Cntn1a)是哺乳动物中Contactin1(F3/F11/Contactin)的斑马鱼同源物,是神经元和少突胶质细胞的免疫球蛋白超家族识别分子。我们描述了斑马鱼发育中的视通路中少突胶质细胞中明显的Cntn1a mRNA表达。在成体中,这种表达仅保留在视网膜内视神经纤维层的胶质细胞中,该层含有“疏松”髓磷脂。视神经损伤后,少突胶质细胞独立于再生轴突的存在重新表达Cntn1a mRNA,视网膜神经节细胞将Cntn1a表达上调至显著高于发育期间的水平。脊髓损伤后,轴突切断的脑干神经元和脊髓白质胶质细胞中Cntn1a mRNA的表达同样增加。此外,erbB3缺陷型突变幼虫三叉神经/前侧线神经节中mRNA表达降低,这意味着Cntn1a在雪旺细胞分化中起作用。这些复杂的调控模式表明Cntn1a在髓鞘形成细胞和神经元中发挥作用,特别是在中枢神经系统的成功再生中。

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