Date of Completion
Honors College Thesis
J Matthew Mahoney
epilepsy, seizures, astrocytes, GFAP
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.
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Milligan, Harriet R., "Exploring the Potential Role of Reactive Astrocytosis in Cognitive Impairments from Early Life Seizures" (2020). UVM Honors College Senior Theses. 354.