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
