Abstract
The mechanisms responsible for the dopamine deficit in Lesch Nyhan Disease (LND) and in the HPRT-knockout mouse are poorly understood. We have used microarray transcriptional profiling methods to characterize global patterns of gene expression in the striatum of wild type and HPRT-knockout mice to test our hypothesis that secondary genetic aberrations play a role in the altered CNS function in this disease. We have used the murine full genome GeneChip Mouse Genome 430 2.0 arrays and have identified a small number of genes (>2 fold difference) whose expression in the striatum becomes more than two-fold aberrantly expressed as determined by gene expression studies and as confirmed by quantitative PCR during the 4-8 weeks of post-natal life.
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