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First published online 10 November 2004
doi: 10.1242/dev.01532

Development 131, 6023-6031 (2004)
Published by The Company of Biologists 2004
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{alpha}3ß1 integrin modulates neuronal migration and placement during early stages of cerebral cortical development

Ralf S. Schmid1, Stephanie Shelton2, Amelia Stanco1, Yukako Yokota1, Jordan A. Kreidberg3 and E. S. Anton1,*

1 UNC Neuroscience Center and the Department of Cell and Molecular Physiology, The University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA
2 Department of Biological Sciences, Stanford University, Stanford, CA 94305, USA
3 Department of Medicine, Children's Hospital, Boston and Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA

* Author for correspondence (e-mail: anton{at}med.unc.edu)

Accepted 29 September 2004

We show that {alpha}3 integrin mutation disrupts distinct aspects of neuronal migration and placement in the cerebral cortex. The preplate develops normally in {alpha}3 integrin mutant mice. However, time lapse imaging of migrating neurons in embryonic cortical slices indicates retarded radial and tangential migration of neurons, but not ventricular zone-directed migration. Examination of the actin cytoskeleton of {alpha}3 integrin mutant cortical cells reveals aberrant actin cytoskeletal dynamics at the leading edges. Deficits are also evident in the ability of developing neurons to probe their cellular environment with filopodial and lamellipodial activity. Calbindin or calretinin positive upper layer neurons as well as the deep layer neurons of {alpha}3 integrin mutant mice expressing EGFP were misplaced. These results suggest that {alpha}3ß1 integrin deficiency impairs distinct patterns of neuronal migration and placement through dysregulated actin dynamics and defective ability to search and respond to migration modulating cues in the developing cortex.

Key words: Cerebral cortex, Migration, Adhesion




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