Abstract
Abstract Spinal cord injury (SCI) can induce dysfunction in a multitude of neural circuits including those that lead to impaired sleep, respiratory dysfunction, and neuropathic pain. We used a lower thoracic rodent contusion SCI model of neuropathic pain that has been shown to associate with increased spontaneous activity in primary afferents and hindlimb mechanosensory stimulus hypersensitivity. Here we paired capture of these variables with chronic capture of three state sleep and respiration to more broadly understand SCI-induced physiological dysfunction and to assess possible interrelations. Noncontact electric field sensors were embedded into home cages to non-invasively capture the temporal evolution of sleep and respiration changes for six weeks after SCI in naturally behaving mice. Hindlimb mechanosensitivity was assessed weekly, and terminal experiments measured primary afferent spontaneous activity in situ from intact lumbar dorsal root ganglia (DRG). We observed that SCI led to increased spontaneous primary afferent activity (both firing rate and the number of spontaneously active DRGs) that correlated with increased respiratory rate variability and measures of sleep fragmentation. This is the first study to measure and link sleep dysfunction and variability in respiratory rate in a SCI model of neuropathic pain, and thereby provide broader insight into the magnitude of overall stress burden initiated by neural circuit dysfunction after SCI.