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

• Published in: Neurologia (Barcelona, Spain) Vol. 32; no. 9; p. 587
• Main Authors: Rincón-López, C, Tlapa-Pale, A, Medel-Matus, J-S, Martínez-Quiroz, J, Rodríguez-Landa, J F, López-Meraz, M-L
• Format: Journal Article
• Language: English
• Published: Spain 01.11.2017
• Subjects: Age Factors; Animals; Cell Death; Dentate Gyrus - drug effects; Dentate Gyrus - pathology; Disease Models, Animal; Female; Hippocampus - drug effects; Hippocampus - pathology; Injections, Intraventricular; Interleukin 1 Receptor Antagonist Protein - administration & dosage; Interleukin-1beta - administration & dosage; Male; Neurons; Rats; Rats, Wistar; Status Epilepticus; Estado epiléptico; Giro dentado; Hipocampo; Dentate gyrus; Muerte neuronal; Rata en desarrollo; Interleucina-1β; Interleukin-1β; Neuronal cell death; Developing rat; Status epilepticus; Hippocampus
• ISSN: 1578-1968
• DOI: 10.1016/j.nrl.2016.03.013

Interleukin-1β (IL-1β) increases necrotic neuronal cell death in the CA1 area after induced status epilepticus (SE) in developing rats. However, it remains uncertain whether IL-1β has a similar effect on the hippocampal dentate gyrus (DG). In this study, we analysed the effects of IL-1β on 14-day-old Wistar rats experiencing DG neuronal death induced by SE. SE was induced with lithium-pilocarpine. Six hours after SE onset, a group of pups was injected with IL-1β (at 0, 0.3, 3, 30, or 300ng/μL) in the right ventricle; another group was injected with IL-1β receptor (IL-1R1) antagonist (IL-1Ra, at 30ng/μL) of IL-1RI antagonist (IL-1Ra) alone, and additional group with 30ng/μL of IL-1Ra plus 3ng/μL of IL-1β. 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. We observed an increased number of eosinophilic cells in the hippocampal DG ipsilateral to the site of injection of 3ng/μL and 300ng/μL of IL-1β in comparison with the vehicle group. A similar effect was observed in the hippocampal DG contralateral to the site of injection of 3ng/μL of IL-1β. Administration of both of IL-1β and IL-1Ra failed to prevent an increase in the number of eosinophilic cells. Our data suggest that IL-1β increases apoptotic neuronal cell death caused by SE in the hippocampal GD, which is a mechanism independent of IL-1RI activation.