Visual Recovery Following Optic Nerve Crush in Male and Female Wild-type and TRIF Deficient Mice 公开

Abstract

Optic Nerve Injury induces neurodegeneration both in the retina and in the visual structures of the brain and some of the major signaling pathways involved in this type of injury have been identified. In addition to the identified pathways, the TIR-domain-containing interferon- β (TRIF) adapting solely to toll-like receptors (TLR)-3, may also play an important role in post-optic nerve crush (ONC) neurodegeneration of the optic nerve and retina, due to its mediation of inflammatory TLR3 signaling when overexpressed. In this study, we hypothesize that mice with the TRIF gene knocked out will demonstrate decreased inflammatory responses and greater recovery from ONC. We found that TRIF knockout mice had reduced inflammation and neurodegeneration, better neuroprotection in the retina and optic nerves and, better recovery of visual function following ONC compared to those of wild type mice. This study allows us to gain more understanding of the role of TRIF pathway in the optic nerve regeneration and retinal neurodegeneration. Since the TRIF pathway is commonly involved in the innate immune response in the brain, our study will also further clarify its role in the central nervous system.

Table of Contents

I.            Introduction ……………………………………………………………………… 1

II.          Methods ………………………………………………………………………….  4

III.         Results …………………………………………………………………………...  11

IV.         Discussion ……………………………………………………………………….  19

V.          References ……………………………………………………………………….  27

About this Honors Thesis

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School	Emory College
Department	Neuroscience and Behavioral Biology
Degree	B.S.
Submission	Honors Thesis
Language	English
Research Field	Biology, Neuroscience
关键词	optic nerve crush TRIF toll like receptor pathway nerve regeneration toll-like-receptor 3
Committee Chair / Thesis Advisor	Donald G. Stein, Emory University
Committee Members	Michael Iuvone, Emory University Elena Sergeeva, Harvard Children's Hospital Robert Wyttenbach, Emory University

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