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早期胚胎神经元在未成熟和成年中枢神经系统组织上的广泛体外再生。

Extensive regeneration in vitro by early embryonic neurons on immature and adult CNS tissue.

作者信息

Shewan D, Berry M, Cohen J

机构信息

Division of Anatomy and Cell Biology, UMDS, London, UK.

出版信息

J Neurosci. 1995 Mar;15(3 Pt 1):2057-62. doi: 10.1523/JNEUROSCI.15-03-02057.1995.

Abstract

The failure of axon regeneration in the injured adult CNS has been ascribed to axon growth inhibitory molecules expressed by the resident glial cell populations, especially oligodendrocytes. Unlike their adult counterparts, however, early embryonic neurons are able to send lengthy axons through myelinated fiber tracts when transplanted into the adult brain. One explanation is that they have yet to express receptors for factors that inhibit the growth of older neurons. To test this possibility, we have used the cryoculture technique to study the regeneration of rat central and peripheral neurons, over a developmental period that encompasses the stages before, during, and after target contact, when cultured on either unmyelinated (neonatal) or myelinated (adult) optic nerve tissue sections. Early embryonic (days 14-15) retinal ganglion cells extended neurites on neonatal optic nerve, but few grew on adult optic nerve. In the case of early embryonic dorsal root ganglion neurons, however, neurite outgrowth on either neonatal optic nerve or on adult optic nerve was extensive. This response declined sharply with age. In contrast, neurite outgrowth by dorsal root ganglion neurons on laminin substrata remained relatively constant (> 80% extended neurites) over the same period. This suggests that (a) inhibition of neurite outgrowth within the optic nerve is mediated not only by oligodendrocytes, but also by molecules expressed prior to the onset of myelination; (b) neurons acquire receptors for these inhibitors only late in embryonic development; (c) differences exist between developing central and peripheral neurons in the response to myelin-associated axon-growth inhibitors.

摘要

成年中枢神经系统损伤后轴突再生失败被归因于驻留神经胶质细胞群体(尤其是少突胶质细胞)表达的轴突生长抑制分子。然而,与成年神经元不同,早期胚胎神经元移植到成年大脑时能够通过有髓纤维束发出长轴突。一种解释是它们尚未表达抑制较成熟神经元生长的因子的受体。为了验证这种可能性,我们使用冷冻培养技术研究大鼠中枢和外周神经元在一个涵盖靶标接触之前、期间和之后阶段的发育时期内,培养于无髓鞘(新生)或有髓鞘(成年)视神经组织切片上时的再生情况。早期胚胎(第14 - 15天)视网膜神经节细胞在新生视神经上伸出神经突,但在成年视神经上很少生长。然而,对于早期胚胎背根神经节神经元,在新生视神经或成年视神经上的神经突生长都很广泛。这种反应随年龄急剧下降。相比之下,在同一时期,背根神经节神经元在层粘连蛋白基质上的神经突生长保持相对稳定(> 80%伸出神经突)。这表明:(a)视神经内神经突生长抑制不仅由少突胶质细胞介导,还由髓鞘形成开始之前表达的分子介导;(b)神经元仅在胚胎发育后期才获得这些抑制剂的受体;(c)发育中的中枢和外周神经元对髓鞘相关轴突生长抑制剂的反应存在差异。

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