Melatonin is neuroprotective in experimental Streptococcus pneumoniae meningitis.

Neuronal injury in bacterial meningitis is a consequence of the direct toxicity of bacterial components and inflammatory and oxidative mechanisms. Adjunctive therapy with melatonin was investigated in vitro and in experimental meningitis. Cellular damage was reduced by treatment with melatonin in organotypic hippocampal cultures (P<.

Clindamycin is neuroprotective in experimental Streptococcus pneumoniae meningitis compared with ceftriaxone.

In animal models of Streptococcus pneumoniae meningitis, rifampin is neuroprotective in comparison to ceftriaxone. So far it is not clear whether this can be generalized for other protein synthesis-inhibiting antimicrobial agents. We examined the effects of the bactericidal protein synthesis-inhibiting clindamycin (n = 12) on the release of proinflammatory bacterial components, the formation of neurotoxic compounds and neuronal injury compared with the standard therapy with ceftriaxone (n = 12) in a rabbit model of pneumococcal meningitis.

Increased neurogenesis after experimental Streptococcus pneumoniae meningitis.

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.

Differential regulation of Toll-like receptor mRNAs in experimental murine central nervous system infections.

Toll-like receptors (TLR) play a key role in the recognition of microbial components. We investigated the differential regulation of TLR mRNA expression in bacterial and viral mouse models of central nervous system infection. Streptococcus pneumoniae meningitis led to an enhanced expression of TLR2, TLR4 and TLR9 mRNA.

Neurotoxicity of pneumolysin, a major pneumococcal virulence factor, involves calcium influx and depends on activation of p38 mitogen-activated protein kinase.

Neuronal injury in bacterial meningitis is caused by the interplay of host inflammatory responses and direct bacterial toxicity. We investigated the mechanisms by which pneumolysin, a cytosolic pneumococcal protein, induces damage to neurons. The toxicity after exposure of human SH-SY5Y neuroblastoma cells and hippocampal organotypic cultures to pneumolysin was time- and dose-dependent.

Spatio-temporal Distribution of Epileptiform Potentials in the Hippocampal Slice: Recordings with Voltage-sensitive Dyes.

Voltage-sensitive dyes and fast optical recording techniques were used to monitor the spatio-temporal activity pattern of epileptiform potentials in hippocampal slices from guinea pigs. Epileptiform potentials were induced by adding 4-aminopyridine to the bath solution and applying single pulse stimulation either to the stratum pyramidale of area CA3 or to the stratum radiatum of area CA1. Optical activity as well as intra- or extracellular electrical activity were recorded from area CA1.