Cortical development in the presenilin-1 null mutant mouse fails after splitting of the preplate and is not due to a failure of reelin-dependent signaling
Version of Record online: 26 AUG 2008
Copyright © 2008 Wiley-Liss, Inc.
Volume 237, Issue 9, pages 2405–2414, September 2008
How to Cite
De Gasperi, R., Gama Sosa, M. A., Wen, P. H., Li, J., Perez, G. M., Curran, T. and Elder, G. A. (2008), Cortical development in the presenilin-1 null mutant mouse fails after splitting of the preplate and is not due to a failure of reelin-dependent signaling. Dev. Dyn., 237: 2405–2414. doi: 10.1002/dvdy.21661
- Issue online: 26 AUG 2008
- Version of Record online: 26 AUG 2008
- Manuscript Accepted: 16 JUN 2008
- National Institute on Aging. Grant Numbers: AG020139, AG029361
- National Alliance for Research in Schizophrenia and Affective Disorders (NARSAD)
Additional Supporting Information may be found in the online version of this article.
|SuppFigS1.tif||1793K||Supplemental Fig 1. Calretinin immunostaining reveals splitting of the preplate in <I>Psen1−/−</I> telencephalon. Coronally cut Vibratome sections from E15.5 wild type (A, C, E) or <I>Psen−/−</I> embryos (B, D, F) were immunostained for calretinin (red) along with a DAPI nuclear stain (blue). Sections through the lateral telencephalon are shown labeled for DAPI (A, B), immunostained for calretinin (C, D) or as a merged image (E, F). The marginal zone (MZ), cortical plate (CP), subplate region (SP) and intermediate zone (IZ) are indicated. Scale bar: 100 μm|
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