You are not currently logged in.
Access JSTOR through your library or other institution:
If You Use a Screen ReaderThis content is available through Read Online (Free) program, which relies on page scans. Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Reelin, Disabled 1, and β1 Integrins Are Required for the Formation of the Radial Glial Scaffold in the Hippocampus
Eckart Förster, Albrecht Tielsch, Barbara Saum, Karl Heinz Weiss, Celine Johanssen, Diana Graus-Porta, Ulrich Müller and Michael Frotscher
Proceedings of the National Academy of Sciences of the United States of America
Vol. 99, No. 20 (Oct. 1, 2002), pp. 13178-13183
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/3073369
Page Count: 6
You can always find the topics here!Topics: Neuroglia, Stripes, Neurons, Mice, Scaffolds, Dentate gyrus, Receptors, Integrins, Cultured cells, Antibodies
Were these topics helpful?See something inaccurate? Let us know!
Select the topics that are inaccurate.
Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Preview not available
The extracellular matrix molecule Reelin is required for the correct positioning of neurons during the development of the forebrain. However, the mechanism of Reelin action on neuronal migration is poorly understood. Reelin is assumed to act on neurons directly, but it may also affect the differentiation of glial cells necessary for neuronal migration. Here we show that a regular glial scaffold fails to form in vivo in the dentate gyrus of mice deficient of Reelin or Disabled 1, a neuronal adaptor protein in the Reelin signaling pathway. A subset of these defects is observed in mice that lack β1-class integrins, known to bind Reelin. Moreover, recombinant Reelin induced branching of glial processes in vitro. Our data suggest that Reelin affects glial differentiation via Disabled 1 and β1-class integrin-dependent signaling pathways.
Proceedings of the National Academy of Sciences of the United States of America © 2002 National Academy of Sciences