International Mammalian Genome Society


The 13th International Mouse Genome Conference
October 31-November 3, 1999

Table of Contents * Structure * Bioinformatics * Sequence * Mapping * New Tools * Gene Discovery * Developmental * Mutagenesis * Functional Genomics

G9 Developmental Profile of Abnormal Cerebellar Development in Ts65Dn Mice

Laura L. Baxter and Roger H. Reeves. Department of Physiology, Johns Hopkins School of Medicine, Baltimore, MD 21205

Ts65Dn mice are at dosage imbalance for most of the same genes as individuals with Down syndrome (DS). Several phenotypes in these mice parallel those in DS, including a deficit in learning and memory measured in the Morris Swim Maze; craniofacial anomalies arising from disruption of the same skeletal elements; and a small cerebellum. Not only do Ts65Dn mice display the same significant overall reduction in cerebellum as in DS, but Ts65Dn mice also serve an instructional role in revealing new phenotypes of DS. This was shown by the discovery of reduced granule (gc) density in Ts65Dn mice, and the subsequent identification of reduced gc density in the DS cerebellum as well (Baxter et al., submitted).

Given the precise recapitulation of the DS cerebellar phenotype in adult Ts65Dn mice, a post-natal developmental profile was performed to determine the time course of this maldevelopment. This study represents the first quantitative developmental analysis of the brain in Ts65Dn mice. Mice were analyzed at the day of birth (P0), P6, P14, and P23-24. Sagittal sections were taken at the midline, and the total area of the cerebellum was measured and related to the total brain area in cross section. The thickness of the cellular layers, the gc density, and the rates of gc apoptosis were also examined. The results show that during these postnatal developmental stages, Ts65Dn mice are characterized by a growth delay and with reduced brain weight through earlier developmental stages. Specific aspects of developmental delay of the cerebellum were quantitated by the measurements of the Ts65Dn cerebellum described above. These data provide the basis for understanding the developmental processes underlying the neurological anomalies characteristic of DS.

 


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