Reuß, Bernhard M.

[["dc.bibliographiccitation.firstpage","316"],["dc.bibliographiccitation.journal","Brain Research"],["dc.bibliographiccitation.lastpage","332"],["dc.bibliographiccitation.volume","1184"],["dc.contributor.author","Koester-Patzlaff, Christiane"],["dc.contributor.author","Hosseini, Seyed Mehdi"],["dc.contributor.author","Reuss, Bernhard"],["dc.date.accessioned","2018-11-07T10:45:04Z"],["dc.date.available","2018-11-07T10:45:04Z"],["dc.date.issued","2007"],["dc.description.abstract","Neonatal Borna Disease Virus (BDV) infection of the Lewis rat brain leads to dentate gyrus (DG) degeneration, underlying mechanisms are not fully understood. Since astroglial gap junction (GJ) coupling is known to influence neurodegenerative processes, the question arose whether persistent BDV infection influences astroglial connexins (Cx) Cx43 and Cx30 in the hippocampal formation (HiF) of Lewis rats. RT-PCR and Western blot analysis of forebrain (FB) samples revealed a virus dependent reduction of both Cx types 8 but not 4 weeks post infection (p.i.). Immunohistochemistry revealed an increase of Cx43 in the DG and a decrease in the CA3 region 4 and 8 weeks p.i. Cx30, which was detectable only 8 weeks p.i., revealed a BDV dependent increase in DG and CA3 regions. BDV dependent astrogliosis as revealed by immunodetection of glial fibrillary acidic protein (GFAP) correlated not with astroglial connexin expression. With regard to functional coupling as revealed by scrape loading, BDV infection resulted in increased spreading of the GJ permeant dye Lucifer yellow in primary hippocampal astroglial cultures, and in increased expression of Cx43 and Cx30 as revealed by immunocytochemistry. In conclusion, persistent BDV infection of the Lewis rat brain leads to changes in astroglial Cx expression both in vivo and in vitro and of functional coupling in vitro. Distribution and time course of these changes suggest them to be a direct result of neurodegeneration in the DG and an indirect effect of neuronal deafferentiation in the CA3 region. (c) 2007 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.brainres.2007.09.062"],["dc.identifier.isi","000252096600036"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47413"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1872-6240"],["dc.relation.issn","0006-8993"],["dc.title","Persistent Borna Disease Virus infection changes expression and function of astroglial gap junctions in vivo and in vitro"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","78"],["dc.bibliographiccitation.journal","European Journal of Cell Biology"],["dc.bibliographiccitation.lastpage","79"],["dc.bibliographiccitation.volume","85"],["dc.contributor.author","Koester-Patzlaff, Christiane"],["dc.contributor.author","Reuß, Bernhard M."],["dc.date.accessioned","2018-11-07T10:11:30Z"],["dc.date.available","2018-11-07T10:11:30Z"],["dc.date.issued","2006"],["dc.identifier.isi","000237127500169"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40058"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Gmbh, Urban & Fischer Verlag"],["dc.publisher.place","Jena"],["dc.relation.conference","29th Annual Meeting of the German Society for Cell Biology"],["dc.relation.eventlocation","Braunschweig, GERMANY"],["dc.title","Differential changes of gap junction expression in dentate gyrus and cornu ammonis of rats neonatally infected with the Borna disease virus"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","143"],["dc.bibliographiccitation.journal","Brain Research"],["dc.bibliographiccitation.lastpage","158"],["dc.bibliographiccitation.volume","1219"],["dc.contributor.author","Koester-Patzlaff, Christiane"],["dc.contributor.author","Hosseini, Seyed Mehdi"],["dc.contributor.author","Reuss, Bernhard"],["dc.date.accessioned","2018-11-07T11:13:00Z"],["dc.date.available","2018-11-07T11:13:00Z"],["dc.date.issued","2008"],["dc.description.abstract","Neonatal Borna Disease Virus (BDV) infection of the Lewis rat brain, leads to Purkinje cell degeneration, in association with astroglial activation. Since astroglial gap junctions (GJ) are known to influence neuronal degeneration, we investigated BDV dependent changes in astroglial GJ connexins (Cx) Cx43, and Cx30 in the Lewis rat cerebellum, 4, and 8 weeks after neonatal infection. On the mRNA level, RT-PCR demonstrated a BDV dependent increase in cerebellar Cx43, and a decrease in Cx30,8, but not 4 weeks p.i. On the protein level, Western blot analysis revealed no overall upregulation of Cx43, but an increase of its phosphorylated forms, 8 weeks p.i. Cx30 protein was downregulated. Immunohistochemistry revealed a BDV dependent reduction of Cx43 in the granular layer (GL), 4 weeks p.i. 8 weeks p.i., Cx43 immunoreactivity recovered in the GL, and was induced in the molecular layer (ML). Cx30 revealed a BDV dependent decrease in the GL, both 4, and 8 weeks p.i. Changes in astroglial Cxs correlated not with expression of the astrogliotic marker GFAP, which was upregulated in radial glia. With regard to functional coupling, primary cerebellar astroglial cultures, revealed a BDV dependent increase of Cx43, and Cx30 immunoreactivity and in spreading of the GJ permeant dye Lucifer Yellow. These results demonstrate a massive, BDV dependent reorganization of astroglial Cx expression, and of functional GJ coupling in the cerebellar cortex, which might be of importance for the BDV dependent neurodegeneration in this brain region. (C) 2008 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.brainres.2008.04.062"],["dc.identifier.isi","000257907000016"],["dc.identifier.pmid","18538309"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53795"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1872-6240"],["dc.relation.issn","0006-8993"],["dc.title","Layer specific changes of astroglial gap junctions in the rat cerebellar cortex by persistent Borna Disease Virus infection"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","118"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Chemical Neuroanatomy"],["dc.bibliographiccitation.lastpage","127"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Koester-Patzlaff, Christiane"],["dc.contributor.author","Hosseini, Seyed Mehdi"],["dc.contributor.author","Reuss, Bernhard"],["dc.date.accessioned","2018-11-07T08:32:14Z"],["dc.date.available","2018-11-07T08:32:14Z"],["dc.date.issued","2009"],["dc.description.abstract","Neonatal Borna disease virus (BDV) infection of the Lewis rat leads to progressive degeneration of dentate gyrus granule cells, and cerebellar Purkinje neurons. Our aim here was to clarify whether BDV interfered with the formation of electrical synapses. and we, therefore, analysed expression of the neuronal gap junction protein connexin36 (Cx36) in the Lewis rat hippocampal formation, and cerebellar cortex, 4 and 8 weeks after neonatal infection. Semiquantitative RT-PCR. revealed a BDV-dependent decrease in Cx36 mRNA in the hippocampal formation 4 and 8 weeks post-infection (p.i.), and in the cerebellar cortex 8 weeks p.i. Correspondingly, immunofluorescent staining revealed reduced Cx36 immunoreactivity in both dentate gyrus, and ammons horn CA3 region, 4 and 8 weeks post-infection. In the cerebellar cortex, Cx36 immunoreactivity was detected only 8 weeks post-infection in the molecular layer, where it was down regulated by BDV. Our findings demonstrate, for the first time, distinct BDV-dependent reductions in Cx36 mRNA and protein in the rat hippocampal formation and cerebellar cortex, suggesting altered neuronal network properties to be an important feature of persistent viral brain infections. (C) 2008 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jchemneu.2008.10.004"],["dc.identifier.isi","000263623300008"],["dc.identifier.pmid","19038327"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17291"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0891-0618"],["dc.title","Loss of connexin36 in rat hippocampus and cerebellar cortex in persistent Borna disease virus infection"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]