Microglial Activation and Neuronal Apoptosis in Bornavirus Infected Neonatal Lewis Rats
Lewis rats neonatally infected with Borna disease virus have a behavioral syndrome characterized by hyperactivity, movement disorders, and abnormal social interactions. Virus is widely distributed in brain; however, neuropathology is focused in dentate gyrus, cerebellum, and neocortex where granule...
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| Veröffentlicht in: | Brain pathology (Zurich, Switzerland) Switzerland), 2000-04, Vol.10 (2), p.260-272 |
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| creator | Weissenböck, Herbert Hornig, Mady Hickey, William F. Lipkin, W. Ian |
| description | Lewis rats neonatally infected with Borna disease virus have a behavioral syndrome characterized by hyperactivity, movement disorders, and abnormal social interactions. Virus is widely distributed in brain; however, neuropathology is focused in dentate gyrus, cerebellum, and neocortex where granule cells, Purkinje cells and pyramidal cells are lost through apoptosis. Although a transient immune response is present, its distribution does not correlate with sites of damage. Neuropathology is instead colocalized with microglial proliferation and expression of MHC class I and class II, ICAM, CD4 and CD8 molecules. Targeted pathogenesis in this system appears to be linked to microglial activation and susceptibility of specific neuronal populations to apoptosis rather than viral tropism or virus‐specific immune responses. |
| doi_str_mv | 10.1111/j.1750-3639.2000.tb00259.x |
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Ian</creatorcontrib><title>Microglial Activation and Neuronal Apoptosis in Bornavirus Infected Neonatal Lewis Rats</title><title>Brain pathology (Zurich, Switzerland)</title><addtitle>Brain Pathol</addtitle><description>Lewis rats neonatally infected with Borna disease virus have a behavioral syndrome characterized by hyperactivity, movement disorders, and abnormal social interactions. Virus is widely distributed in brain; however, neuropathology is focused in dentate gyrus, cerebellum, and neocortex where granule cells, Purkinje cells and pyramidal cells are lost through apoptosis. Although a transient immune response is present, its distribution does not correlate with sites of damage. Neuropathology is instead colocalized with microglial proliferation and expression of MHC class I and class II, ICAM, CD4 and CD8 molecules. Targeted pathogenesis in this system appears to be linked to microglial activation and susceptibility of specific neuronal populations to apoptosis rather than viral tropism or virus‐specific immune responses.</description><subject>Animals</subject><subject>Animals, Newborn - physiology</subject><subject>Antigens - metabolism</subject><subject>Apoptosis - physiology</subject><subject>Borna Disease - metabolism</subject><subject>Borna Disease - pathology</subject><subject>Borna Disease - physiopathology</subject><subject>Borna disease virus</subject><subject>Borna disease virus - genetics</subject><subject>Borna disease virus - metabolism</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>Disease Models, Animal</subject><subject>Microglia - metabolism</subject><subject>Microglia - physiology</subject><subject>Neurons - physiology</subject><subject>Nucleoproteins - metabolism</subject><subject>Phenotype</subject><subject>Rats</subject><subject>Rats, Inbred Lew - physiology</subject><subject>RNA, Viral - metabolism</subject><subject>Time Factors</subject><subject>Tissue Distribution</subject><subject>Viral Proteins - metabolism</subject><issn>1015-6305</issn><issn>1750-3639</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkVFv0zAUhSMEYmPwF1DEEy8J13HsxDwgtQXGUBkwQHu8chxnuKRxsZ2u-_c4alXGI36x5fvd4-tzkuQFgZzE9WqVk4pBRjkVeQEAeWgACiby3YPk9Fh6GM9AWMYpsJPkifcrACK4YI-TEwIVL6Fkp8n1J6OcvemN7NOZCmYrg7FDKoc2vdSjs8N0v7GbYL3xqRnSuXWD3Bo3-vRi6LQKeiIjFyK51LeRupLBP00edbL3-tlhP0t-vH_3ffEhW34-v1jMlpnipIRMCqCsLAvedA0XpRKFZqJuO6I5UNGUlAhNailoSykoEUloIwmFprLpFKNnyZu97mZs1rpVeghO9rhxZi3dHVpp8N_KYH7ijd1iDaIuRRUFXh4EnP09ah9wbbzSfS8HbUePJI4XjWM1RPT1Ho2Oee90d3yGAE7J4Aon-3GyH6dk8JAM7mLz8_uD3mvdR_H3J7em13f_IY3zL7OCT-NlewHjg94dBaT7hbyiFcPry3O8qt6W3-ZfP-KC_gFcUq5b</recordid><startdate>200004</startdate><enddate>200004</enddate><creator>Weissenböck, Herbert</creator><creator>Hornig, Mady</creator><creator>Hickey, William F.</creator><creator>Lipkin, W. Ian</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>5PM</scope></search><sort><creationdate>200004</creationdate><title>Microglial Activation and Neuronal Apoptosis in Bornavirus Infected Neonatal Lewis Rats</title><author>Weissenböck, Herbert ; Hornig, Mady ; Hickey, William F. ; Lipkin, W. Ian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6140-a90354426bfb694c92e598df1e6039b4319e18a93d330c94420dfb602e3abfc53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Animals</topic><topic>Animals, Newborn - physiology</topic><topic>Antigens - metabolism</topic><topic>Apoptosis - physiology</topic><topic>Borna Disease - metabolism</topic><topic>Borna Disease - pathology</topic><topic>Borna Disease - physiopathology</topic><topic>Borna disease virus</topic><topic>Borna disease virus - genetics</topic><topic>Borna disease virus - metabolism</topic><topic>Brain - metabolism</topic><topic>Brain - pathology</topic><topic>Disease Models, Animal</topic><topic>Microglia - metabolism</topic><topic>Microglia - physiology</topic><topic>Neurons - physiology</topic><topic>Nucleoproteins - metabolism</topic><topic>Phenotype</topic><topic>Rats</topic><topic>Rats, Inbred Lew - physiology</topic><topic>RNA, Viral - metabolism</topic><topic>Time Factors</topic><topic>Tissue Distribution</topic><topic>Viral Proteins - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Weissenböck, Herbert</creatorcontrib><creatorcontrib>Hornig, Mady</creatorcontrib><creatorcontrib>Hickey, William F.</creatorcontrib><creatorcontrib>Lipkin, W. Ian</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Brain pathology (Zurich, Switzerland)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Weissenböck, Herbert</au><au>Hornig, Mady</au><au>Hickey, William F.</au><au>Lipkin, W. Ian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Microglial Activation and Neuronal Apoptosis in Bornavirus Infected Neonatal Lewis Rats</atitle><jtitle>Brain pathology (Zurich, Switzerland)</jtitle><addtitle>Brain Pathol</addtitle><date>2000-04</date><risdate>2000</risdate><volume>10</volume><issue>2</issue><spage>260</spage><epage>272</epage><pages>260-272</pages><issn>1015-6305</issn><eissn>1750-3639</eissn><abstract>Lewis rats neonatally infected with Borna disease virus have a behavioral syndrome characterized by hyperactivity, movement disorders, and abnormal social interactions. Virus is widely distributed in brain; however, neuropathology is focused in dentate gyrus, cerebellum, and neocortex where granule cells, Purkinje cells and pyramidal cells are lost through apoptosis. Although a transient immune response is present, its distribution does not correlate with sites of damage. 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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Animals Animals, Newborn - physiology Antigens - metabolism Apoptosis - physiology Borna Disease - metabolism Borna Disease - pathology Borna Disease - physiopathology Borna disease virus Borna disease virus - genetics Borna disease virus - metabolism Brain - metabolism Brain - pathology Disease Models, Animal Microglia - metabolism Microglia - physiology Neurons - physiology Nucleoproteins - metabolism Phenotype Rats Rats, Inbred Lew - physiology RNA, Viral - metabolism Time Factors Tissue Distribution Viral Proteins - metabolism |
| title | Microglial Activation and Neuronal Apoptosis in Bornavirus Infected Neonatal Lewis Rats |
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