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多种机制促使感觉轴突避开禽类表皮。

Multiple mechanisms contribute to the avoidance of avian epidermis by sensory axons.

作者信息

Cahoon S M, Scott S A

机构信息

Program in Neuroscience and Department of Neurobiology and Anatomy, University of Utah School of Medicine, 50 North Medical Drive, Salt Lake City, Utah, 84132, USA.

出版信息

Dev Biol. 1999 Apr 15;208(2):502-12. doi: 10.1006/dbio.1999.9220.

DOI:10.1006/dbio.1999.9220
PMID:10191062
Abstract

In birds, sensory innervation of skin is restricted to dermis, with few axons penetrating into the epidermis. This pattern of innervation is maintained in vitro, where sensory neurites avoid explants of epidermis but grow readily on dermis. We have used this coculture paradigm to investigate the mechanisms that impede innervation of avian epidermis. The lack of epidermal innervation in birds has been attributed to diffusible chondroitin sulfate proteoglycans (CSPGs) secreted by the epidermis, although direct experimental evidence is weak. We found that elimination of CSPG function with either chondroitinase or neutralizing antibodies did not promote growth of DRG neurites onto epidermis in vitro, indicating that CSPGs alone are not responsible for preventing epidermal innervation. Moreover, the failure of sensory neurites to invade epidermis is not due exclusively to soluble chemorepulsive factors, since sensory neurites also avoid dead epidermis. This inhibition can be overridden, however, by coating epidermis with the growth-promoting molecule laminin, but only if the tissue is killed first. Epidermal innervation of laminin-coated epidermis is even more robust when CSPGs are also eliminated. Thus, the absence of growth-promoting or permissive molecules, such as laminin, may contribute to the failure of sensory neurites to invade avian epidermis. Together these results show that the inhibitory character of avian epidermis is complex. Cell- or matrix-associated CSPGs clearly contribute to the inhibition, but are not solely responsible.

摘要

在鸟类中,皮肤的感觉神经支配仅限于真皮,只有少数轴突穿透进入表皮。这种神经支配模式在体外得以维持,在体外,感觉神经突会避开表皮外植体,但在真皮上能轻易生长。我们利用这种共培养模式来研究阻碍鸟类表皮神经支配的机制。鸟类表皮缺乏神经支配一直被归因于表皮分泌的可扩散硫酸软骨素蛋白聚糖(CSPG),尽管直接的实验证据并不充分。我们发现,用软骨素酶或中和抗体消除CSPG功能并不能促进背根神经节(DRG)神经突在体外向表皮生长,这表明仅CSPG并非阻止表皮神经支配的原因。此外,感觉神经突未能侵入表皮并非完全由于可溶性化学排斥因子,因为感觉神经突也会避开死亡的表皮。然而,只有在组织先被杀死的情况下,用促生长分子层粘连蛋白包被表皮才能克服这种抑制作用。当CSPG也被消除时,层粘连蛋白包被的表皮的神经支配甚至更强健。因此,缺乏促生长或允许性分子,如层粘连蛋白,可能导致感觉神经突无法侵入鸟类表皮。这些结果共同表明,鸟类表皮的抑制特性很复杂。细胞或基质相关的CSPG显然对这种抑制有作用,但并非唯一原因。

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