IMR Press / FBE / Volume 8 / Issue 3 / DOI: 10.2741/E775

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article

Immediate epileptogenesis: Impact on brain in C57BL/6J mouse kainate model

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1 Department of Biomedical Sciences, College of Veterinary Medicine, Iowa State University, Ames IA 50011-1250, USA

*Author to whom correspondence should be addressed.

Academic Editor: Ravindra Singh

Front. Biosci. (Elite Ed) 2016, 8(3), 390–411; https://doi.org/10.2741/E775
Published: 1 June 2016
(This article belongs to the Special Issue Pre-mRNA splicing and human diseases)
Abstract

We have recently demonstrated immediate epileptogenesis in the C57BL/6J mouse, the strain that is resistant to kainate-induced neurotoxicity. By using a repeated low dose of kainate, we produced mild and severe status epilepticus (SE) models. In the present study, we demonstrate the impact of mild and severe SE, and spontaneous convulsive/nonconvulsive seizures (CS/NCS) on structure and function of the hippocampus, entorhinal cortex, and amygdala at 7, 14 and 28 day post-SE. Immunohistochemistry (IHC) of brain sections confirmed reactive astrogliosis and microgliosis, neurodegeneration, and increased neurogenesis in both groups. The epileptiform spike rate was higher in the severe group during first 12 days, but they decreased thereafter. Morris water maze test confirmed cognitive deficit in both mild and severe groups at 12d post-SE. However, MRI and IHC at 18 weeks did not reveal any changes in the hippocampus. These findings suggest that in C57BL/6J mice, immediate spontaneous CS could be responsible for early brain pathology or vice versa, however, the persistent spontaneous NCS for a long-term had no impact on the brain structure in both groups.

Keywords
Epileptogenesis
Gliosis
Neurodegeneration
Neurogenesis
Cognitive Deficits
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