Interleukin-1β increases neuronal death in the hippocampal dentate gyrus associated with status epilepticus in the developing rat

Background: Interleukin-1 beta (IL-1 beta) increases necrotic neuronal cell death in the CA1 area after induced status epilepticus (SE) in developing rats. However, it remains uncertain whether IL-1 beta has a similar effect on the hippocampal dentate gyrus (DG). In this study, we analysed the effects of IL-1 beta on 14-day-old Wistar rats experiencing DG neuronal death induced by SE. Methods: SE was induced with lithium-pilocarpine. Six hours after SE onset, a group of pups was injected with IL-1 beta (at 0, 0.3, 3, 30, or 300 ng/mu L) in the right ventricle; another group was injected with IL-1 beta receptor (IL-1R1) antagonist (IL-1Ra, at 30 ng/mu L) of IL-1RI antagonist (IL-1Ra) alone, and additional group with 30 ng/mu L of IL-1Ra plus 3 ng/mu L of IL-1 beta. Twenty-four hours after SE onset, neuronal cell death in the dentate gyrus of the dorsal hippocampus was assessed using haematoxylin-eosin staining. Dead cells showed eosinophilic cytoplasm and condensed and fragmented nuclei. Results: We observed an increased number of eosinophilic cells in the hippocampal DG ipsilateral to the site of injection of 3 ng/mu L and 300 ng/mu L of IL-1 beta in comparison with the vehicle group. A similar effect was observed in the hippocampal DG contralateral to the site of injection of 3 ng/mu L of IL-1 beta. Administration of both of IL-1 beta and IL-1Ra failed to prevent an increase in the number of eosinophilic cells. Conclusion: Our data suggest that IL-1 beta increases apoptotic neuronal cell death caused by SE in the hippocampal GD, which is a mechanism independent of IL-1RI activation. (C) 2016 Sociedad Espanola de Neurologia. Published by Elsevier Espana, S.L.U.