Exacerbated XXXX and acute cell loss, but no changes in epileptogenesis, in @entity19 with increased @entity9140 signaling.

@entity9140 @entity410 @entity4889 @entity19 @entity45770 @entity4176 @entity302 @entity26304 @entity528
Several studies suggest that @entity9140 ( @entity9140 ) can exacerbate @entity410 development during @entity4889 (S.E.) and subsequent epileptogenesis in the adult brain. On the other hand, evidence exists for the protective effect of @entity9140 . To study this controversy, we induced S.E. with @entity4176 in @entity19 with increased @entity9140 signaling due to @entity26304 overexpression. @entity19 experienced a more severe S.E. than wild type animals did. Furthermore, they had increased acute hippocampal neuronal loss when assessed at 48 h after S.E. The effect of @entity26304 overexpression on the development of @entity302 , chronic @entity528 , mossy fiber sprouting, and neurogenesis were studied at 4.5 months after @entity4176 -induced S.E. No differences were found in the rate of epileptogenesis, severity of @entity302 , or cellular markers of network reorganization between transgenic and wild type @entity19 . No differences between genotypes were observed in @entity45770 staining, indicating no effect of @entity26304 overexpression to immature neuron numbers. Instead, in Cresyl Violet-stained preparations, the highest density of neurons was found in untreated @entity19 suggesting a favorable effect of @entity26304 overexpression on the survival of neurons in the hippocampus. Our data support the role of @entity9140 and @entity26304 signaling in @entity410 generation and acute cellular damage after S.E. Long-term outcome was not, however, exacerbated by @entity26304 overexpression.
