Cerebral Cortex Advance Access first published online on December 27, 2006
This version published online on January 17, 2007
Cerebral Cortex, doi:10.1093/cercor/bhl146
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Involvement of the Myelin-Associated Inhibitor Nogo-A in Early Cortical Development and Neuronal Maturation
1 Department of Cell Biology, Cellular and Molecular Basis of Neurodegeneration and Neurorepair, 2 Neurobiology of Development and Regeneration, Institute for Research in Biomedicine and Department of Cell Biology, Barcelona Science Park, University of Barcelona, Josep Samitier 1-5, 08028 Barcelona, Spain, 3 Department of Neurosciences, University of California San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0691, USA
Address correspondence to Ana Mingorance-Le Meur, PhD, Department of Cellular and Physiological Sciences, University of British Columbia–Life Sciences Institute, 2350 Health Sciences Mall, Vancouver, BC V6T 1Z3, Canada. Email: alemeur{at}interchange.ubc.ca or to José A. del Rio, PhD, Neurobiology of Development and Regeneration, Institute for Research in Biomedicine and Department of Cell Biology, Barcelona Science Park, University of Barcelona, Josep Samitier 1–5, 08028 Barcelona, Spain. Email: jadelrio{at}pcb.ub.es.
Nogo-A is a myelin-associated protein expressed by neurons and myelinating mature oligodendrocytes in the central nervous system. Although most research has focused on the participation of Nogo-A in the prevention of axonal regeneration and plasticity in the adult, little attention has been paid to the putative functions of Nogo-A during embryonic development. Here we examined the general pattern and cell-specific distribution of Nogo-A in the prenatal mouse telencephalon. In addition, we studied the development of the major axon tracts and radial and tangential migration in Nogo-A/B/C knockout mice. The pattern of Nogo-A showed distinct distribution in radial glia and postmitotic neurons, in which it is particularly enriched in developing axons. Similarly, Nogo-A was enriched at the leading process of tangentially migrating interneurons but not detectable in radial migrating neurons. Although a low level of Nogo-A appears to be on the surface of many cortical neurons, most proteins have intracellular localization. In Nogo-deficient background, neurons displayed early polarization and increased branching in vitro, probably reflecting a cell-intrinsic role of Nogo proteins in branching reduction, and early tangential migration was delayed. On the basis of these observations, we propose that Nogo proteins, particularly Nogo-A, are involved in multiple processes during cortical development.
Key Words: axon tract • Nogo • radial glia • tangential migration
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