Date of Last Revision

2023-05-02 18:55:14



Degree Name

Bachelor of Science

Date of Expected Graduation

Spring 2016


Metabolic Syndrome is a human condition that presents with various metabolic issues such as abnormal distribution of body fat, high blood pressure, and a prothrombotic state, among other problems (Alberti,et al, 2005). This syndrome is a risk factor for visual disorders, such as glaucoma, and is often associated with increased levels of neuroinflammation. Currently, the animal model used to replicate this syndrome is The Low Capacity Runner and High Capacity Runner Rat Model. These rats have been bred based on their running capacities for 30+ generations to have drastic metabolic differences. We assessed key areas of the retinal ganglion cell projection (optic nerve, superior colliculus, and retina) and other important thalamic nuclei in Metabolic Syndrome such as the arcuate nuclei and inferior colliculus, in the rats for expression of glial fibrillary acidic protein and Aquaporin 4. We expected to find elevated glial fibrillary acidic protein and Aquaporin 4 in key visual structures of Low Capacity Runner compared to High Capacity Runner rats. We found that in the superior colliculi of the Low Capacity Runner rats there was significantly a greater percent area fraction of glial fibrillary acidic protein than in the High Capacity Runner rats; as there was little Aquaporin 4 staining in many of the regions assessed, that data was inconclusive and it appears Aquaporin 4 plays a negligible role in stress-related changes associated with the Metabolic Syndrome phenotype. In this research, we provide novel evidence that Low Capacity Runner rats express an elevated immune response compared to their High Capacity Runner counterparts and that this response is partially specific to visual structures, as the inferior colliculus, an auditory-related thalamic nuclei, shoed to astroglial differences between High Capacity Runners and Low Capacity Runners. These findings could lead to a better understanding of the metabolic underpinnings of optic neuropathies and present new avenues for their treatment.

Research Sponsor

Dr. James Holda

First Reader

Dr. Samuel Crish

Second Reader

Dr. Jordan Renna

20160426104227237.pdf (34 kB)
Signature Page for Research Project

Poster-Final.jpg (3962 kB)



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