Date of Completion

7-11-2018

Embargo Period

7-6-2018

Advisors

Dr. Eric Levine and Dr. Stephen Crocker

Field of Study

Biomedical Science

Degree

Master of Science

Open Access

Open Access

Abstract

Spinal cord injury (SCI) results in varying degrees of paralysis, loss of normal sensory function and, oftentimes, chronic pain originating below the level of injury. Post-SCI pain tends to be resistant to traditional analgesic therapies and has been shown to impair recovery of function, making it a significant healthcare concern. Approximately one third of SCI patients report abdominal pain as a primary and severe symptom with marked similarity to other functional gastrointestinal pain disorders (e.g. irritable bowel). The etiology of this intense pain phenotype is unclear given that visceral organs are left uninjured in SCI. Here we examine changes in expression of pain-relevant genes in the colon following SCI both over time and between two different specific injury parameters. Mice underwent spinal contusion injury resulting in complete paralysis below the level of the forelimbs (two injury severity conditions), were then sacrificed 1 or 7 days following SCI, and alterations in pain-relevant gene expression were determined using quantitative RT-PCR. Additionally, the presence of inflammation at 1 day post-SCI was performed using hematoxylin and eosin staining. The data indicate a pattern of both time- and injury-dependent differential gene expression within the colon following SCI including Gfrα1-3, Trkb, Trkc, Asic1, Asic2, and Calcα. Further, pilot hematoxylin and eosin studies suggest that differences in expression in the first 24 hours post-injury may be inflammation independent. Differentially expressed genes in the periphery may offer insight into novel therapeutic targets for prevention and treatment of abdominal pain following SCI.

Major Advisor

Dr. Erin Young

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