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Cerebral Cortex Advance Access originally published online on November 26, 2008
Cerebral Cortex 2009 19(8):1857-1869; doi:10.1093/cercor/bhn213
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© The Author 2008. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Cortical Interneurons Require p35/Cdk5 for their Migration and Laminar Organization

Sonja Rakic1, Yuchio Yanagawa2, Kunihiko Obata3, Clare Faux1, John G. Parnavelas1 and Margareta Nikolic4

1 Department of Anatomy and Developmental Biology, University College London, London WC1E 6BT, UK, 2 Department of Genetic and Behavioral Neuroscience, Gunma University Graduate School of Medicine, 3-39-22 Showa-machi, Maebashi 371-8511, Japan, 3 Neuronal Circuit Mechanisms Research Group, RIKEN Brain Science Institute, Wako 351-0198, Japan, 4 Department of Cellular and Molecular Neuroscience, Division of Neuroscience and Mental Health, Imperial College Faculty of Medicine, London W12 0NN, UK

Address correspondence to Margareta Nikolic, Department of Cellular and Molecular Neuroscience, Division of Neuroscience and Mental Health, Burlington Dane's Building, Imperial College School of Medicine, Hammersmith Campus, Du Cane Road, London W12 0NN, UK. Email: m.nikolic{at}imperial.ac.uk.

Projection neurons and interneurons populate the cerebral cortex in a layer-specific manner. Here, we studied the role of Cyclin-dependent kinase 5 (Cdk5) and its activator p35 in cortical interneuron migration and disposition in the cortex. We found that mice lacking p35 (p35–/–) show accumulation of interneurons in the upper part of the cortex. We also observed an inverted distribution of both early- and late-born interneurons, with the former showing a preference for the upper and the latter for the lower aspects of the cortex. We investigated the causes of the altered laminar organization of interneurons in p35–/– mice and found a cell-autonomous delay in their tangential migration that may prevent them from reaching correct positions. Incomplete splitting of the preplate in p35–/– mice, which causes accumulation of cells in the superficial layer and defects in the "inward" and "outward" components of their radial movement, may also account for the altered final arrangement of interneurons. We, therefore, propose that p35/Cdk5 plays a key role in guiding cortical interneurons to their final positions in the cortex.

Key Words: cortex • development • layering • preplate layer • tangential migration


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