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The Journal of Neuroscience, October 11, 2006, 26(41):10452-10460; doi:10.1523/JNEUROSCI.2850-06.2006

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Neurobiology of Disease
A Progressive and Cell Non-Autonomous Increase in Striatal Neural Stem Cells in the Huntington's Disease R6/2 Mouse

Claudia M. C. Batista,^1,2 * Tod E. Kippin,^1,3 * Sandrine Willaime-Morawek,¹ Marília Kimie Shimabukuro,² Wado Akamatsu,¹ and Derek van der Kooy¹

¹Neurobiology Research Group, Department of Medical Genetics and Microbiology, University of Toronto, Toronto, Ontario, Canada M5S 3E1, ²Departmento de Histologia e Embriologia, Instituto de Ciências Biomédicas, Centro de Ciências da Saúde, Universidade Federal do Rio de Janeiro, 21941-590 Rio de Janeiro, Brazil, and ³Department of Psychology, University of California, Santa Barbara, Santa Barbara, California 93106-9660

Correspondence should be addressed to Dr. Derek van der Kooy, Department of Medical Genetics and Microbiology, University of Toronto, 160 College Street, Centre for Cellular and Biomolecular Research, Room 1102, Toronto, Ontario, Canada M5S 3E1. Email: derek.van.der.kooy{at}utoronto.ca

Neural stem and progenitor cells are located in the subependyma of the adult forebrain. An increase in adult subependymal cell proliferation is reported after various kinds of brain injury. We demonstrate an expansion of neural precursor cells in the postnatal subependyma in a murine genetic disease model of Huntington's disease (HD), the R6/2 mouse. We used the in vitro neurosphere assay as an index of the number of neural stem cells in vivo and to assess proliferation kinetics in vitro and in vivo bromodeoxyuridine labeling to assess the progenitor cell population and their fates. Disease progression in this model leads to an increase in the numbers of neural stem cells in the adult striatal subependyma. This increase is produced cell non-autonomously by events in the R6/2 brains as the mice become increasingly symptomatic. Once the neural stem cell increase is induced in vivo, it is maintained during in vitro passaging of neural stem cells, but the neural stem cell increase is not reproduced during in vitro passaging of neural stem cells from presymptomatic R6/2 mice. In addition, we show that some of the R6/2 neural progenitor cells show a change from their normal migration destiny toward the olfactory bulb. Instead, some of these cells migrate into the striatum, one of the main affected areas in HD. Our findings demonstrate that HD damage recruits precursor cells in two ways: expansion of neural stem cells and altered migration of progenitor cells.

Key words: neural stem cells; progenitor cells; Huntington's disease; subependyma; migration; R/2 mice

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Received Dec. 21, 2005; revised Aug. 28, 2006; accepted Aug. 29, 2006.

Correspondence should be addressed to Dr. Derek van der Kooy, Department of Medical Genetics and Microbiology, University of Toronto, 160 College Street, Centre for Cellular and Biomolecular Research, Room 1102, Toronto, Ontario, Canada M5S 3E1. Email: derek.van.der.kooy{at}utoronto.ca

Related articles in J. Neurosci.:

Proliferating Neural Precursor Cells as First Step toward Neuroregeneration in Huntington's Disease?

Mannie M. Y. Fan and Jing Fan
J. Neurosci. 2006 26: 13411-13412. [Full Text]  

This article has been cited by other articles:

				M. M. Y. Fan and J. Fan Proliferating Neural Precursor Cells as First Step toward Neuroregeneration in Huntington's Disease? J. Neurosci., December 27, 2006; 26(52): 13411 - 13412. [Full Text] [PDF]

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