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Abstract

SUMMARY OF COMMUNICATIONS CELL DAMAGE AND NEUROGENESIS IN THEDENTATE GRANULE CELL LAYER OF ADULT RATSAFTER PILOCARPINE- OR KAINATE-INDUCEDSTATUS EPILEPTICUS CovolanL.,RibeiroL.T.C.,LongoB.M.andMelloL.E.A.M. Department of Physiology, UNIFESP, 04023-900 Sao Paulo,SP.Presented by A.C.M.Paiva Dentate granule cells are generally considered to berelatively resistant to excitotoxicity and have been asso-ciated to robust synaptogenesis after neuronal damage.Synaptic reorganization of dentate granule cell axons,the mossy fibers, has been suggested to be relevant forhyperexcitability in human temporal lobe epilepsy andanimal models. A recent hypothesis has suggested thatmossy fiber sprouting is dependent on newly formed den-tate granule cells. However, we have recently demon-strated that cycloheximide (CHX) can block the mossyfiber sprouting that would be otherwise induced by dif-ferent epileptogenic agents and do not interfere withepileptogenesis in those models. Here, we investigatedcell damage and neurogenesis in the dentate gyrus ofpilocarpine- or kainate-treated animals with or withoutthe co-administration of CHX. Dentate granule cells werehighly vulnerable to pilocarpine induced-status epilep-ticus (SE), but hardly damaged by kainate induced-SE.CHX-pretreatment markedly reduced the number of in-jured neurons after pilocarpine-induced SE. Induction ofSE dramatically increased the mitotic rate of KA and KA+ CHX treated animals. Induction of SE in animals in-jected with pilocarpine alone led to increases of betweentwo to sevenfold in the mitotic rate of dentate granulecells as compared to increases of between five and thirty-fold for pilocarpine+CHX animals. These observationsindicate that in presence of cycloheximide the increase ofthe mitotic rate after pilocarpine-induced SE may be duetoprotectionofavulnerableprecursorcellpopulationthatwould otherwise degenerate. We further suggest that themossy fiber sprouting and neurogenesis of granule cellsare not necessarily related events. — ( September 14,1999 ).