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PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2008-6-27
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
11
pubmed:volume
1219
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
143-58
pubmed:meshHeading
pubmed-meshheading:18538309-Animals, pubmed-meshheading:18538309-Animals, Newborn, pubmed-meshheading:18538309-Borna Disease, pubmed-meshheading:18538309-Borna disease virus, pubmed-meshheading:18538309-Cells, Cultured, pubmed-meshheading:18538309-Cerebellar Cortex, pubmed-meshheading:18538309-Connexin 43, pubmed-meshheading:18538309-Connexins, pubmed-meshheading:18538309-Disease Models, Animal, pubmed-meshheading:18538309-Female, pubmed-meshheading:18538309-Gap Junctions, pubmed-meshheading:18538309-Gene Expression Regulation, Viral, pubmed-meshheading:18538309-Glial Fibrillary Acidic Protein, pubmed-meshheading:18538309-Male, pubmed-meshheading:18538309-Neuroglia, pubmed-meshheading:18538309-Pregnancy, pubmed-meshheading:18538309-RNA, Messenger, pubmed-meshheading:18538309-Rats, pubmed-meshheading:18538309-Rats, Inbred Lew, pubmed-meshheading:18538309-Time Factors
pubmed:year
2008
pubmed:articleTitle
Layer specific changes of astroglial gap junctions in the rat cerebellar cortex by persistent Borna Disease Virus infection.
pubmed:affiliation
Center for Anatomy, Neuroanatomy, University of Göttingen, Kreuzbergring 36, 37075 Göttingen, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't