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- W1880770180 abstract "Astrocytes have been proposed to have multiple roles in the development and maintenance of the vertebrate CNS. To facilitate documentation of these roles, we designed a transgene to enable their ablation at selectable times. The transgene consists of the coding region for the herpes simplex virus-thymidine kinase (HSV-TK) under the control of the human glial fibrillary acidic protein gene promoter. The HSV-TK is innocuous but converts the antiherpetic agent ganciclovir (GCV) to a toxic product that interferes with DNA replication in proliferating cells. In a developmental study, transgenic mice were treated with GCV during the first postnatal week, with evaluation at P19. Treated mice displayed severe ataxia. Histological examination revealed disrupted astrocyte development, particularly in the cerebellum, with marked secondary effects on other cell types. Cerebellar defects included a loss in the numbers of astrocytes and an overall reduction in cerebellar size and disruption of the normally well defined cellular layers. Radial glia were disordered, Purkinje cells were ectopically distributed and displayed abnormal dendritic trees, and granule cells were markedly depleted. These effects were more severe in animals treated on postnatal day 1 versus treatment at day 5. A major factor causing granule cell death was excitotoxicity attributable to activation of NMDA receptors. These results suggest a critical role for astrocytes in cerebellar development." @default.
- W1880770180 created "2016-06-24" @default.
- W1880770180 creator A5005531623 @default.
- W1880770180 creator A5013180945 @default.
- W1880770180 creator A5080356197 @default.
- W1880770180 date "1996-11-01" @default.
- W1880770180 modified "2023-10-12" @default.
- W1880770180 title "Conditional Ablation of Cerebellar Astrocytes in Postnatal Transgenic Mice" @default.
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- W1880770180 doi "https://doi.org/10.1523/jneurosci.16-21-06908.1996" @default.
- W1880770180 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6579279" @default.
- W1880770180 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/8824329" @default.
- W1880770180 hasPublicationYear "1996" @default.