| pubmed-article:17182680 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17182680 | lifeskim:mentions | umls-concept:C0042769 | lld:lifeskim |
| pubmed-article:17182680 | lifeskim:mentions | umls-concept:C0021289 | lld:lifeskim |
| pubmed-article:17182680 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
| pubmed-article:17182680 | lifeskim:mentions | umls-concept:C0034143 | lld:lifeskim |
| pubmed-article:17182680 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:17182680 | lifeskim:mentions | umls-concept:C1514562 | lld:lifeskim |
| pubmed-article:17182680 | lifeskim:mentions | umls-concept:C1883221 | lld:lifeskim |
| pubmed-article:17182680 | lifeskim:mentions | umls-concept:C0205345 | lld:lifeskim |
| pubmed-article:17182680 | lifeskim:mentions | umls-concept:C0333467 | lld:lifeskim |
| pubmed-article:17182680 | lifeskim:mentions | umls-concept:C0936012 | lld:lifeskim |
| pubmed-article:17182680 | lifeskim:mentions | umls-concept:C1883204 | lld:lifeskim |
| pubmed-article:17182680 | lifeskim:mentions | umls-concept:C1880389 | lld:lifeskim |
| pubmed-article:17182680 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:17182680 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:17182680 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:17182680 | pubmed:dateCreated | 2007-2-26 | lld:pubmed |
| pubmed-article:17182680 | pubmed:abstractText | Infection of newborn Lewis rats with Borna disease virus (neonatal Borna disease [NBD]) results in cerebellar damage without the cellular inflammation associated with infections in later life. Purkinje cell (PC) damage has been reported for several models of early-life viral infection, including NBD; however, the time course and distribution of PC pathology have not been investigated rigorously. This study examined the spatiotemporal relationship between PC death and zonal organization in NBD cerebella. Real-time PCR at postnatal day 28 (PND28) revealed decreased cerebellar levels of mRNAs encoding the glycolytic enzymes aldolase C (AldoC, also known as zebrin II) and phosphofructokinase C and the excitatory amino acid transporter 4 (EAAT4). Zebrin II and EAAT4 immunofluorescence analysis in PND21, PND28, PND42, and PND84 NBD rat cerebella revealed a complex pattern of PC degeneration. Early cell loss (PND28) was characterized by preferential apoptotic loss of zebrin II/EAAT4-negative PC subsets in the anterior vermis. Consistent with early preferential loss of zebrin II/EAAT4-negative PCs in the vermis, the densities of microglia and the Bergmann glial expression of metallothionein I/II and the hyaluronan receptor CD44 were higher in zebrin II/EAAT4-negative zones. In contrast, early loss in lateral cerebellar lobules did not reflect a similar discrimination between PC phenotypes. Patterns of vermal PC loss became more heterogeneous at PND42, with the loss of both zebrin II/EAAT4-negative and zebrin II/EAAT4-positive neurons. At PND84, zebrin II/EAAT4 patterning was abolished in the anterior cerebellum, with preferential PC survival in lobule X. Our investigation reveals regional discrimination between patterns of PC subset loss, defined by zebrin II/EAAT4 expression domains, following neonatal viral infection. These findings suggest a differential vulnerability of PC subsets during the early stages of virus-induced neurodegeneration. | lld:pubmed |
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| pubmed-article:17182680 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17182680 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17182680 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17182680 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
