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lüll Spatiotemporal analysis of purkinje cell degeneration relative to parasagittal expression domains in a model of neonatal viral infection Williams BL; Yaddanapudi K; Hornig M; Lipkin WIJ Virol 2007[Mar]; 81 (6): 2675-87Infection 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.|*Borna disease virus[MESH]|Animals[MESH]|Animals, Newborn[MESH]|Borna Disease/*metabolism/pathology[MESH]|Calbindins[MESH]|Cell Death[MESH]|Cerebellum/physiopathology[MESH]|Excitatory Amino Acid Transporter 4/analysis/metabolism[MESH]|Fluorescent Antibody Technique, Indirect[MESH]|Kinetics[MESH]|Models, Neurological[MESH]|Nerve Tissue Proteins/analysis/metabolism[MESH]|Oligonucleotide Array Sequence Analysis[MESH]|Phosphofructokinase-1, Type C/analysis/metabolism[MESH]|Polymerase Chain Reaction[MESH]|Purkinje Cells/*physiology[MESH]|RNA, Messenger/analysis[MESH]|Rats[MESH]|Rats, Inbred Lew[MESH]|S100 Calcium Binding Protein G/metabolism[MESH] |