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Vol. 28, No. 1-2, 2006
Issue release date: February 2006
Section title: Original Paper
Dev Neurosci 2006;28:102–117
(DOI:10.1159/000090757)

Notch1 Signaling Influences V2 Interneuron and Motor Neuron Development in the Spinal Cord

Yang X. · Tomita T. · Wines-Samuelson M. · Beglopoulos V. · Tansey M.G. · Kopan R. · Shen J.
aCenter for Neurologic Diseases, Brigham and Women’s Hospital, Program in Neuroscience, Harvard Medical School, Boston, Mass., bDepartment of Molecular Biology and Pharmacology, and Division of Dermatology, Department of Medicine, Washington University School of Medicine, St. Louis, Mo., and cDepartment of Physiology, The University of Texas Southwestern Medical Center at Dallas, Dallas, Tex., USA

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: 2/16/2005
Accepted: 6/21/2005
Published online: 3/3/2006

Number of Print Pages: 16
Number of Figures: 6
Number of Tables: 0

ISSN: 0378-5866 (Print)
eISSN: 1421-9859 (Online)

For additional information: http://www.karger.com/DNE

Abstract

The Notch signaling pathway plays a variety of roles in cell fate decisions during development. Previous studies have shown that reduced Notch signaling results in premature differentiation of neural progenitor cells, while increased Notch activities promote apoptotic death of neural progenitor cells in the developing brain. Whether Notch signaling is involved in the specification of neuronal subtypes is unclear. Here we examine the role of Notch1 in the development of neuronal subtypes in the spinal cord using conditional knockout (cKO) mice lacking Notch1 specifically in neural progenitor cells. Notch1 inactivation results in accelerated neuronal differentiation in the ventral spinal cord and gradual disappearance of the ventral central canal. These changes are accompanied by reduced expression of Hes1 and Hes5 and increased expression of Mash1 and Neurogenin 1 and 2. Using markers (Nkx2.2, Nkx6.1, Olig2, Pax6 and Dbx1) for one or multiple progenitor cell types, we found reductions of all subtypes of progenitor cells in the ventral spinal cord of Notch1 cKO mice. Similarly, using markers (Islet1/2, Lim3, Sim1, Chox10, En1 and Evx1/2) specific for motor neurons and distinct classes of interneurons, we found increases in the number of V0–2 interneurons in the ventral spinal cord of Notch1 cKO mice. Specifically, the number of Lim3+/Chox10+ V2 interneurons is markedly increased while the number of Lim3+/Islet+motor neurons is decreased in the Notch1 cKO spinal cord, suggesting that V2 interneurons are generated at the expense of motor neurons in the absence of Notch1. These results provide support for a role of Notch1 in neuronal subtype specification in the ventral spinal cord.


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: 2/16/2005
Accepted: 6/21/2005
Published online: 3/3/2006

Number of Print Pages: 16
Number of Figures: 6
Number of Tables: 0

ISSN: 0378-5866 (Print)
eISSN: 1421-9859 (Online)

For additional information: http://www.karger.com/DNE


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Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in goverment regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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