No difference in number, severity and duration of seizures between groups. No effect on doublecortin-expressing neuronal progenitor cells, and no effect on subpopulation of these cells with persistent basal dendrites compared to vehicle control. No endo-N effect on hilar basal dendrite generation compared to vehicle control. This was confirmed by structural studies which showed that the endoneuraminidase-sensitive brain material consisted of multimers of sialic acid. ![]() However, endo-N treatment reduces the total number of newborn neurons (64%) upon induction of the status epileptics compared to vehicle treatment. ![]() Increase of newborn cells in status epileptics rats compared to controls without significant difference between endo-N and vehicle treatment. Specific alteration of NCAM-mediated cell adhesion by an endoneuraminidase. In the current study, we used light-induced retinal degeneration (LIRD) as a model to investigate whether NCAM plays a functional role in neuroprotection and whether NCAM influences p75NTR signaling in modulating retinal cell survival. Almost complete removal of polysialic acid by endo-N injection into the brain 5 days after stimulation (return to normal polysialic acid levels after 11 weeks): no effect on proliferation, neurogenesis, and the fate of newborn cells in the hippocampus of rats without status epileptics. Endoneuraminidase-N (Endo-N) can specifically cleave PSA from NCAM.
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