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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Astrocyte-specific TSC1 conditional knockout mice exhibit abnormal neuronal organization and seizures.

Persons affected with tuberous sclerosis complex (TSC) develop a wide range of neurological abnormalities including aberrant neuronal migration and seizures. In an effort to model TSC-associated central nervous system abnormalities in mice, we generated two independent lines of astrocyte-specific Tsc1 conditional knockout mice by using the Cre-LoxP system. Astrocyte-specific Tsc1-null mice exhibit electroencephalographically proven seizures after the first month of age and begin to die at 3 to 4 months. Tsc1-null mice show significant increases in astrocyte numbers throughout the brain by 3 weeks of age and abnormal neuronal organization in the hippocampus between 3 and 5 weeks. Moreover, cultured Tsc1-null astrocytes behave similar to wild-type astrocytes during log phase growth but demonstrate increased saturation density associated with reduced p27(Kip1) expression. Collectively, our results demonstrate that astrocyte-specific disruption of Tsc1 in mice provides a context-dependent growth advantage for astrocytes that results in abnormalities in neuronal organization and epilepsy.[1]

References

  1. Astrocyte-specific TSC1 conditional knockout mice exhibit abnormal neuronal organization and seizures. Uhlmann, E.J., Wong, M., Baldwin, R.L., Bajenaru, M.L., Onda, H., Kwiatkowski, D.J., Yamada, K., Gutmann, D.H. Ann. Neurol. (2002) [Pubmed]
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