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Volume 16, Number 19, Issue of October 1, 1996 pp. 6175-6182
Copyright ©1996 Society for Neuroscience

Consequences of Trisomy 16 for Mouse Brain Development: Corticogenesis in a Model of Down Syndrome

Received April 26, 1996; revised July 1, 1996; accepted July 7, 1996.

Tarik F. Haydar¹, Mary E. Blue^{3, 4}, Mark E. Molliver^{4, 5}, Bruce K. Krueger¹, and Paul J. Yarowsky²

Departments of ¹ Physiology and ² Pharmacology and Experimental Therapeutics, University of Maryland School of Medicine, Baltimore, Maryland 21201, ³ Neuroscience Laboratory, Kennedy-Krieger Research Institute, Baltimore, Maryland 21205, and Departments of ⁴ Neurology and ⁵ Neuroscience, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205

We have studied abnormalities in the tangential and radial expansion of the cerebral cortex during fetal development in the trisomy 16 (Ts16) mouse, a model for human trisomy 21 (Down syndrome). Slowed tangential expansion of the neuroepithelium in Ts16 resulted in a reduction of final telencephalic size and is predicted to decrease the number of radial cortical units in the mature brain. In addition, radial growth of the Ts16 cortex was delayed at the time of peak cortical neurogenesis in normal mice, but by embryonic day 18 the cortex reached normal thickness. Because mouse chromosome 16 shares many genes with human chromosome 21, abnormalities in Ts16 brain development may parallel abnormalities in trisomy 21.

Key words: cerebral cortex; development; histogenesis; Down syndrome; trisomy 16; mental retardation

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