Abstract
Treatment of excitotoxically injured organotypic hippocampal slice cultures (OHSC) with clodronate is known to result in the inhibition of microglial activation. We hypothesized that this is due to direct effects of clodronate on microglial cells, and investigated microglial proliferation in OHSC, and cytokine and NO secretion in isolated microglial cells. N-methyl-D-aspartate (NMDA) lesioning of OHSC resulted in a massive increase in the number of proliferating, bromo-desoxy-uridine (BrdU)-labeled cells that was reduced to control levels after treatment with clodronate (0.1, 1, 10 microg/ml). Triple-labeling revealed that clodronate abrogated the proliferation of both glial fibrillary acidic protein (GFAP)-labeled astrocytes and Griffonia simplicifolia isolectin B4 (IB4)-labeled microglial cells. Furthermore, isolated microglial cells were treated with clodronate after stimulation with lipopolysaccharide (LPS) or macrophage colony stimulating factor (M-CSF). Clodronate (0.01, 0.1, 1 microg/ml) significantly down-regulated the LPS-stimulated microglial secretion of tumor necrosis factor (TNF)-alpha, Interleukin (IL)-1beta and NO, but not of IL-6. In contrast, clodronate significantly reduced the microglial IL-6-release induced ...Continue Reading
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