| Literature DB >> 12898528 |
Joachim Gerber1, Tobias Böttcher, Judith Bering, Stephanie Bunkowski, Wolfgang Brück, Ulrich Kuhnt, Roland Nau.
Abstract
Neuronal damage in the hippocampal formation is a common feature in animal models of bacterial meningitis and human disease. In mouse and rabbit models of Streptococcus pneumoniae meningitis, proliferation of neural progenitor cells quantified by bromodeoxyuridine (BrdU) incorporation was enhanced in the subgranular layer of the dentate gyrus. In mice, the density of BrdU-labeled cells was maximal on Day 2 after infection. Approximately 60% of the cells labeled by BrdU between Days 7 and 10 after infection that remained present 28 days later had migrated into deeper layers of the dentate gyrus and differentiated into neurons, as evidenced by immunohistochemical staining for TUC-4, MAP-2 and beta-tubulin. This suggests that endogenous repair mechanisms may limit consequences of neuronal destruction after meningitis. Copyright 2003 Wiley-Liss, Inc.Entities:
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Year: 2003 PMID: 12898528 DOI: 10.1002/jnr.10682
Source DB: PubMed Journal: J Neurosci Res ISSN: 0360-4012 Impact factor: 4.164