Gerber Joachim, Böttcher Tobias, Bering Judith, Bunkowski Stephanie, Brück Wolfgang, Kuhnt Ulrich, Nau Roland
Department of Neurology, Georg-August-University, Göttingen, Germany.
J Neurosci Res. 2003 Aug 15;73(4):441-6. doi: 10.1002/jnr.10682.
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.