Modulation of growth cone morphology by substrate-bound adhesion molecules.

Modulation of growth cone morphology by substrate-bound adhesion molecules.
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通过基质结合的粘附分子调节生长锥形态。

DOI:
10.1002/cm.970210108
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发表时间:
1992
影响因子:
--
通讯作者:
Lemmon,V
Lemmon,V
中科院分区:
--
文献类型:
--
作者:
Payne,HR;Burden,SM;Lemmon,V

文献摘要

被引文献

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生长锥是轴突发育和再生的末端结构,具有运动和引导功能。在体内,生长锥对环境线索作出反应,以引导轴突到达其适当的靶点。这些线索被认为是负责生长锥中的位置特异性形态学变化,但控制生长锥行为的分子的特征很差。我们使用扫描电子显微镜分析体外视网膜神经节细胞生长锥的形态,轴突通常在体内遇到不同的粘附分子。L1/8D 9、N-钙粘蛋白和层粘连蛋白各自在生长锥中诱导独特的形态学特征。生长锥响应于细胞粘附分子L1/8D 9和N-钙粘蛋白而精心制作了片状伪足结构,而层粘连蛋白支持具有小面纱的丝状伪足生长锥。在L1/8D 9上,生长锥更大,产生更多的丝状伪足。L1/8D 9上相邻生长锥和神经突之间的丝状伪足连接很常见,但层粘连蛋白或N-钙粘蛋白上不常见。这些结果表明,不同的粘附分子对生长锥形态具有深刻不同的影响。这与以前的报告一致,表明生长锥形态在体内发生变化,在基板组成的变化。
The growth cone, a terminal structure on developing and regenerating axons, is specialized for motility and guidance functions. In vivo the growth cone responds to environmental cues to guide the axon to its appropriate target. These cues are thought to be responsible for position‐specific morphological changes in the growth cone, but the molecules that control growth cone behavior are poorly characterized. We used scanning electron microscopy to analyze the morphology of retinal ganglion cell growth cones in vitro on different adhesion molecules that axons normally encounter in vivo. L1/8D9, N‐cadherin, and laminin each induced distinctive morphological characteristics in growth cones. Growth cones elaborated lamellipodial structures in response to the cell adhesion molecules L1/8D9 and N‐cadherin, whereas laminin supported filopodial growth cones with small veils. On L1/8D9, the growth cones were larger and produced more filopodia. Filopodial associations between adjacent growth cones and neurites were frequent on L1/8D9 but were uncommon on laminin or N‐cadherin. These results demonstrate that different adhesion molecules have profoundly different effects on growth cone morphology. This is consistent with previous reports suggesting that changes in growth cone morphology in vivo occur in response to changes in substrate composition.