The effects of brain-irradiation-induced decreases in hippocampal mitotic activity on flurothyl-induced epileptogenesis in adult C57BL/6J mice.

Previous studies have demonstrated that seizures are potent inducers of mitotic activity in the rodent hippocampus. The role of this mitotic activity in epileptogenesis currently remains unknown. In the present study, we investigated the effect of alterations in hippocampal mitotic activity on changes in seizure threshold and phenotype using flurothyl kindling.

Differences in hippocampal mitotic activity within the dorsal and ventral hippocampus following flurothyl seizures in mice.

To date, there is little information regarding the regional division (dorsal and ventral) of hippocampal mitotic activity at either baseline or following seizures. To determine the regional distribution of hippocampal mitotic activity, animals were given seizures followed by injections of 5-bromo-2'-deoxyuridine (label for mitotic cells). Our results indicate that the baseline and seizure-induced levels of mitotic activity (neurogenesis) are greater in the dorsal hippocampus as compared to the ventral hippocampus.

Altered flurothyl seizure induction latency, phenotype, and subsequent mortality in a mouse model of juvenile neuronal ceroid lipofuscinosis/batten disease.

Purpose: Juvenile neuronal ceroid lipofuscinosis (JNCL), or Batten disease, is a pediatric neurodegenerative disease characterized by vision loss, seizure activity, cognitive decline, and premature death. Discovery of the Batten disease-related gene, CLN3, led to creation of a Cln3 protein-deficient mouse model (Cln3-/-), which recapitulates some of the histopathologic characteristics of the human condition. We hypothesized that lack of Cln3 would alter seizure-related behavioral parameters.