Abstract
Bowel dysfunction, is a prevalent and life-impacting comorbidity of spinal cord injury (SCI) with no long-term treatment available. SCI-induced colon changes including motility and fibrosis are understudied as are strategies to address SCI bowel dysfunction. This need remains partly due to the lack of a mouse model that recapitulates the human condition. We hypothesized that a high thoracic spinal transection in mice would trigger bowel dysfunction with coincident colon pathology similar to humans and rats after SCI. We observed bowel dysfunction as increased fecal pellet numbers within the colon, smaller pellet size, and decreased motility. Fecal pellets numbers in the colon increased significantly in SCI animals versus sham (laminectomy only) injuries by 4 days postinjury (dpi) and persisted to 7 and 21 dpi. The number of pellets expelled (fecal output) significantly decreased in SCI versus sham animals at both 7 and 20 dpi. Pellet size was significantly decreased in SCI animals at 7 and 14 dpi, collectively indicative of decreased motility with SCI. SCI caused non-significant reductions in colonic motility (bead expulsion assay) at all three timepoints. Through ex vivo myograph analyses of live colon sections, we detected significant increase in the maximal contractility of the circular musculature from both the proximal and distal colon after SCI at 21 dpi. At the same time point, distal colons displayed significant collagen deposition in the musculature after SCI. Collectively, these findings demonstrate bowel dysfunction immediately after injury that continues in the distal colon over time. Establishing this mouse model enables further interrogation using transgenic models.