Spinal cord injury in neonate rats alters respiratory neural output via supraspinal mechanisms

The primary cause of mortality in spinal cord injured patients is respiratory insufficiency. Upper cervical spinal cord injury (SCI) interrupts descending respiratory motor drive, altering ventilation. Alterations in breathing patterns after SCI are dependent on peripheral feedback mechanisms; however, it is not clear whether supraspinal plasticity also occurs. Alterations in respiratory frequency after SCI could suggest supraspinal plasticity since respiratory frequency is controlled at the brainstem level. We hypothesized that SCI may induce supraspinal respiratory plasticity in rats. Therefore, we examined the effect of C2 hemisection in neonate rats on the respiratory‐like motor output of brainstem‐spinal cord preparations. On postnatal day (P)0 or 1, a C2 hemisection surgery was performed under ketamine/xylazine and cold anesthesia. On P3, P4, or P5, rats (hemisected and littermate controls) were deeply anesthetized with halothane and brainstem‐spinal cords removed. Respiratory‐related activity was recorded from C4 ventral roots while the pH of the superfusate was changed (pH 7.2, 7.4 and 7.8). Respiratory‐like frequency was significantly increased as pH was decreased in both hemisected (n=6) and controls (n=6) (p<0.001). The frequency of respiratory‐like neural discharge was significantly reduced in hemisected rats compared to controls at all pH values (p=0.015). These data suggest that SCI does not alter the sensitivity to pH, but that supraspinal plasticity of the respiratory system occurs in neonate rats since the frequency of the in‐vitro preparation was significantly altered. The mechanisms underlying this supraspinal respiratory plasticity after SCI remain unknown. This research was supported by NIH grant HD 31550