Slit proteins prevent midline crossing and determine the dorsoventral position of major axonal pathways in the mammalian forebrain

被引：356

作者：

Bagri, A

Marín, O

Plump, AS

Mak, J

Pleasure, SJ

Rubenstein, JLR

Tessier-Lavigne, M

机构：

[1] Univ Calif San Francisco, Howard Hughes Med Inst, Dept Anat, San Francisco, CA 94143 USA

[2] Univ Calif San Francisco, Dept Biochem & Biophys, San Francisco, CA 94143 USA

[3] Univ Calif San Francisco, Langley Porter Psychiat Inst, Dept Psychiat, Nina Ireland Lab Dev Neurobiol, San Francisco, CA 94143 USA

[4] Univ Calif San Francisco, Div Med Genet, San Francisco, CA 94143 USA

[5] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA

来源：

NEURON | 2002年 / 33卷 / 02期

关键词：

D O I：

10.1016/S0896-6273(02)00561-5

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

We report that Slit proteins, a family of secreted chemorepellents, are crucial for the proper development of several major forebrain tracts. Mice deficient in Slit2 and, even more so, mice deficient in both Slit1 and Slit2 show significant axon guidance errors in a variety of pathways, including corticofugal, callosal, and thalamocortical tracts. Analysis of multiple pathways suggests several generalizations regarding the functions of Slit proteins in the brain, which appear to contribute to (1) the maintenance of dorsal position by prevention of axonal growth into ventral regions, (2) the prevention of axonal extension toward and across the midline, and (3) the channeling of axons toward particular regions.

引用

页码：233 / 248

页数：16