The Effect of Peripheral Pain on Spinal Circuits Following Spinal Cord Injury

Events soon after spinal cord trauma alter spinal cord function and drastically impact functional outcomes. Guided by our work in a transection model of spinal learning, we hypothesized that uncontrollable noxious input (C fiber activation) undermines spinal function by engaging a pro- inflammatory state (central sensitization). In a clinically relevant model of spinal cord injury (SCI), C fiber input exacerbates inflammatory processes within the lesion, increases cell death, and impairs functional outcomes. However, the mechanisms that underlie increased cell death and inflammation following C fiber activation have not been fully described. Specifically, the extent to which descending, brain-mediated processes are required is unknown. Here, we examined whether local spinal circuits, or descending brain-mediated processes, contribute to the increased inflammation associated with C fiber activation. In a contusion model of SCI, a spinal transection was used to isolate the spinal cord from the brain. Electrical stimulation of the tail provided C fiber activation. Examination of hemoglobin, IL-18, and IL-1β concentrations revealed that complete spinal transection reversed the detrimental effects of C fiber input. These results suggest that brain-mediated processes are required for the development of secondary injury cascades associated with C fiber activation following SCI