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The Journal of Neuroscience, July 11, 2007, 27(28):7397-7407; doi:10.1523/JNEUROSCI.1434-07.2007

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Development/Plasticity/Repair
BMPR1a Signaling Determines Numbers of Oligodendrocytes and Calbindin-Expressing Interneurons in the Cortex

Jayshree Samanta,¹ Gordon M. Burke,¹ Tammy McGuire,¹ Anna J. Pisarek,¹ Abhishek Mukhopadhyay,¹ Yuji Mishina,² and John A. Kessler¹

¹Department of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, and ²Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709

Correspondence should be addressed to John A. Kessler, 303 East Chicago Avenue, Ward 10-233, Chicago, IL 60611. Email: jakessler{at}northwestern.edu

Progenitor cells that express the transcription factor olig1 generate several neural cell types including oligodendrocytes and GABAergic interneurons in the dorsal cortex. The fate of these progenitor cells is regulated by a number of signals including bone morphogenetic proteins (BMPs) secreted in the dorsal forebrain. BMPs signal by binding to heteromeric serine–threonine kinase receptors formed by type I (BMPR1a, BMPR1b, Alk2) and type II (BMPRII) subunits. To determine the specific role of the BMPR1a subunit in lineage commitment by olig1-expressing cells, we used a cre/loxP genetic approach to ablate BMPR1a in these cells while leaving signaling from other subunits intact. There was a reduction in numbers of immature oligodendrocytes in the BMPR1a-null mutant brains at birth. However, by postnatal day 20, the BMPR1a-null mice had a significant increase in the number of mature and immature oligodendrocytes compared with wild-type littermates. There was also an increase in the proportion of calbindin-positive interneurons in the dorsomedial cortex of BMPR1a-null mice at birth without any change in the number of parvalbumin- or calretinin-positive cells. These effects were attributable, at least in part, to a decrease in the length of the cell cycle in subventricular zone progenitor cells. Thus, our findings indicate that BMPR1a mediates the suppressive effects of BMP signaling on oligodendrocyte lineage commitment and on the specification of calbindin-positive interneurons in the dorsomedial cortex.

Key words: BMPR1a; Olig1; calbindin; knock-out mice; oligodendrocyte; stem cell

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Received Sept. 20, 2006; revised May 25, 2007; accepted May 31, 2007.

Correspondence should be addressed to John A. Kessler, 303 East Chicago Avenue, Ward 10-233, Chicago, IL 60611. Email: jakessler{at}northwestern.edu

This article has been cited by other articles:

				J. Jiao and D. F. Chen Induction of Neurogenesis in Nonconventional Neurogenic Regions of the Adult Central Nervous System by Niche Astrocyte-Produced Signals Stem Cells, May 1, 2008; 26(5): 1221 - 1230. [Abstract] [Full Text] [PDF]

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