Date of Award

2021

Document Type

Dissertation/Thesis

Submission Date

October 2026

Thesis/Dissertation Advisor [Chair]

Quan, Ning

Abstract

Epilepsy is a chronic neurological disorder that affects 2.3 million adults and 450,000 children within the US. The etiology of epilepsy is unknown; however, increased severity and neuropathology of epilepsy is associated with inflammatory pathways. Specifically, pro-inflammatory cytokine Interleukin-1 signaling via Interleukin 1 receptor type 1 (IL-1R1) has been shown to decrease sensitivity to kainic acid induced status epilepticus. Our lab hypothesizes that IL-1R1 signaling alters synaptic connectivity in the hippocampus thus conferring increased neuronal excitability. Using WT and IL-1R1 null (Il1r1r/r) mice, colocalization of immunolabeled pre- and post-synaptic markers (VGLUT-1/HOMER1) was analyzed, indicating synapses. Additionally, using the Golgi-Cox method we visualized synaptic spines and analyzed dendritic spine morphology in WT and Il1r1r/r mice. Our results indicate that IL-1R1 does alter synaptic structure suggesting a possible role in the induction of epilepsy. However, these results require further investigation.

Comments

Thesis (B.A.)--Florida Atlantic University, Harriet L. Wilkes Honors College, 2021

Extent

25 p.

Identifier

FAUHT00161

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