Suppr超能文献

调节无长突细胞和视杆光感受器细胞神经突生长的细胞粘附分子。

Cell adhesion molecules regulating neurite growth from amacrine and rod photoreceptor cells.

作者信息

Kljavin I J, Lagenaur C, Bixby J L, Reh T A

机构信息

University of Calgary, Department of Neuroscience, Alberta, Canada.

出版信息

J Neurosci. 1994 Aug;14(8):5035-49. doi: 10.1523/JNEUROSCI.14-08-05035.1994.

Abstract

A great deal is now known about the cell adhesion molecules (CAMs) that are responsible for promoting the growth of ganglion cell axons as they project out of the retina through the optic nerve and finally to distant targets in the brain. However, the CAMs important for regulating axon outgrowth from nonprojection neurons, such as amacrine cells and rods, are not known. Such local circuit neurons extend their neurites rather short distances on cellular surfaces not normally encountered by the ganglion cell axons. To study the mechanisms regulating axon or dendrite growth from local circuit neurons, neurite outgrowth from amacrine cells and rod photoreceptor cells derived from the rat was examined in vitro on immunopurified forms of NCAM, L1, and N-cadherin, three well-characterized adhesive molecules found in the developing retina. Either early (P3) or late (P10) postnatal amacrine cells grew neurites on all three CAMs, but there were significant differences in the percentage of the amacrine cells that responded to each CAM. None of the CAMs supported neurite outgrowth from early postnatal rods, but, surprisingly, NCAM stimulated vigorous neurite extension from rods isolated at postnatal day 10. Postnatal ganglion cells were also examined for comparison and were found not to grow neurites on NCAM, but did grow extensive processes on L1 and N-cadherin. These results show that NCAM, L1, and N-cadherin can promote neurite outgrowth from local circuit neurons, but that the effectiveness of any particular CAM is dependent on the cell type and the developmental period.

摘要

目前,人们对细胞黏附分子(CAMs)已经有了很多了解,这些分子在神经节细胞轴突从视网膜经视神经向外投射并最终到达大脑远处靶点的过程中,负责促进其生长。然而,对于调节无长突细胞和视杆细胞等非投射神经元轴突生长的重要细胞黏附分子,我们还并不清楚。这类局部回路神经元在神经节细胞轴突通常不会遇到的细胞表面上,将其神经突延伸较短的距离。为了研究调节局部回路神经元轴突或树突生长的机制,我们在体外检测了源自大鼠的无长突细胞和视杆光感受器细胞在免疫纯化形式的神经细胞黏附分子(NCAM)、L1和N-钙黏着蛋白上的神经突生长情况,这三种在发育中的视网膜中发现的黏附分子已得到充分表征。出生后早期(P3)或晚期(P10)的无长突细胞在所有三种细胞黏附分子上都能长出神经突,但对每种细胞黏附分子产生反应的无长突细胞百分比存在显著差异。没有一种细胞黏附分子能支持出生后早期视杆细胞的神经突生长,但令人惊讶的是,神经细胞黏附分子能刺激出生后第10天分离的视杆细胞长出旺盛的神经突。作为比较,我们还检测了出生后的神经节细胞,发现它们在神经细胞黏附分子上不会长出神经突,但在L1和N-钙黏着蛋白上能长出广泛的突起。这些结果表明,神经细胞黏附分子、L1和N-钙黏着蛋白可以促进局部回路神经元的神经突生长,但任何一种特定细胞黏附分子的有效性取决于细胞类型和发育时期。

相似文献

引用本文的文献

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验