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The Journal of Neuroscience, October 29, 2003, 23(30):9953-9959

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Development/Plasticity/Repair
Inhibition of Src Family Kinases and Non-Classical Protein Kinases C Induce a Reeler-Like Malformation of Cortical Plate Development

Yves Jossin,¹ Masuhara Ogawa,² Christine Metin,³ Fadel Tissir,¹ and André M. Goffinet¹

¹University of Louvain Medical School, Developmental Genetics Unit, GEDE 7382, B1200 Brussels, Belgium, ²RIKEN–Brain Sciences Institute, 351-0198 Saitama, Japan, and ³U106 Institut National Santé et de la Recherche Médicale, Hôpital Pitié-Salpêtrire, 75651 Paris Cédex 13, France

During development, most cortical neurons migrate to the cortical plate (CP) radially. CP development is abnormal in reeler and other mutant mice with defective Reelin signaling. Reelin is secreted by Cajal-Retzius cells and binds to the very low density lipoprotein receptor and apolipoprotein E receptor type 2 receptors on the surface of CP cells, inducing tyrosine phosphorylation of the intracellular Dab1 adapter. As with Reelin receptors, the identification of Reelin signaling partners is hampered by genetic redundancy. Using a new in vitro embryonic slice culture system, we demonstrate that chemical inhibitors of Src family kinases and Abl, but not inhibitors of Abl alone, generate a reeler-like malformation and that inhibitors of protein kinases C induce a malformation of cortical development that is also reminiscent of reeler. Our observations demonstrate a key role for these enzymes in radial migration to the cortical plate, possibly via interference with Reelin signaling.

Key words: cortex; development; slice; Reelin; tyrosine kinase; protein kinase C

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Received July 3, 2003; revised September 11, 2003; accepted September 13, 2003.

This article has been cited by other articles:

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