Proliferation Changes in Dentate Gyrus of Hippocampus during the First Week following Kainic Acid-induced Seizures

Abstract

Long-term neuroplastic changes in dentate gyrus (DG) have been reported after seizure induction and were shown to contribute to epitogenesis of epilepsy. These changes include increased number of newborn granule cells, sprouted mossyˆbers, granule cell layer dispersion, etc. The aim of current study is to determine the acute progression of neuroplastic changes involved newly generated granule cells after kainic acid (KA)-induced seizures. Doublecortion (DCX) analysis was used to examine the newly generated granule cells morphology 1 7 days after seizure induction. Quantitative analysis of DCX-labeled cells at diŠerent times shows that there are some rapid changes in the dentate gyrus. At day 7 epileptical mice induced an increase of the number of DCX-labeled cells in DG. At days 3 and 7 after epilepsy induction, the percentage of DCX-labeled cells per DG were signiˆcantly increased. These results show that seizures are capable to increase the number of new granule cell within a short time for function activation in post-seizure period. Therefore, the rapid changes in the DG might be having a potential for hippocampus neuroplastic function.

Lipoprotein receptor loss in forebrain radial glia results in neurological deficits and severe seizures

“…The detected impairments included decreased action potential thresholds and increased action potential firing rates (Figure 2f,h), all hallmarks of a hyperexcitable phenotype. In support of our findings, subsequent histology revealed that the upregulation of proliferating cells in the hippocampal dentate gyrus (DG), which is typical for acute phase epilepsy (Gu, Li, Shang, Hou, & Zhao, 2010; Sankar, Shin, Liu, Katsumori, & Wasterlain, 2000), only occurred in P28 KO mice (Figure S4A,B). To further confirm increased excitability and determine affected regions, a P21 KO mouse that suffered from a seizure episode was transcardially perfused 2 hr after seizure onset together with a WT littermate.…”

PI3Kγ deficiency enhances seizures severity and associated outcomes in a mouse model of convulsions induced by intrahippocampal injection of pilocarpine

“…Convulsive stimuli may increase the number of DCX positive cells as early as three days after seizures (Gu et al, 2010;Shapiro et al, 2007a). At this time point, DCX positive newborn cells present basal dendrites phenotype that may form aberrant synapsis in the hilus, contributing to reverberant circuits and epileptogenesis (Shapiro and Ribak, 2006;Shapiro et al, 2007b).…”

“…Moreover, in the present study, we did not use an unbiased stereological method to quantify DCX positive cells, that is a limitation of the approach. Most studies evaluate DCX expression after 3 to 4 weeks after seizures, since a marked increase on hippocampal proliferation after pharmacological induction of seizures in rodents is only detected after 7-9 days after the insult (Gu et al, 2010;Jessberger et al, 2005;Kim et al, 2012;Walter et al, 2007). Interestingly, PI3Kγ −/− animals exhibited a significant decrease in the number of hippocampal DCX + cells after pilocarpine.…”