Date of Completion

2020

Document Type

Honors College Thesis

Department

Neurological Sciences

Thesis Type

Honors College

First Advisor

J Matthew Mahoney

Keywords

epilepsy, seizures, astrocytes, GFAP

Abstract

Childhood epilepsy is often associated with extreme cognitive deficits later in life. Using the repeated flurothyl model, there is the potential to study the behavioral deficits and discover the underlying cause of the cognitive deficits. Reactive astrocytosis, which has been connected to other disease models, was assessed as a potential cause for the behavioral deficits. A twenty-seizure flurothyl protocol was used on C57BL/6J mice at postnatal day ten. Mice either went through a behavior battery once developed or be used for immunohistochemistry one day post seizure, using the glial fibrillary acidic protein (GFAP) marker for reactive astrocytosis. Images were then analyzed using a thresholding code in MATLAB. The mice showed both fear extinction deficits and increased anxiety-like behavior. No differences in astrocyte intensity were found when comparing the seizure and control animals. This suggests reactive astrocytosis may not cause the cognitive deficits observed, but this could be due to intensity not correctly quantifying the differences is astrocytes or a different biological cause all together.

Creative Commons License

Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License.

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