Chronic Spinal Cord Injury Increases Spontaneous Intraspinal Neural Transmission and Spike Train Variability

Spinal cord injury (SCI) often leads to increased spontaneous activity (SpAP) and responsiveness to sensory feedback. This hyperexcitable state contributes to the development and maintenance of SCI-related neuropathic pain (SCI-NP). In general, characterizations of SpAP in the context of SCI-NP focus on the dorsal horns and sensory-processing neurons. As a result, changes in SpAP in the integrative intermediate gray and the motor-dominant ventral horn after SCI are considerably less understood. Thus, it is unclear whether altered firing dynamics in SpAP throughout the dorso-ventral extent of the spinal gray matter contribute to SCI-NP. Here we characterize the firing dynamics of dorsal and ventral interneurons in vivo in neurologically intact rats and rats with chronic SCI with and without SCI-NP. We find (1) robust SpAP throughout the dorsoventral extent of the spinal gray matter after chronic SCI and chronic SCI-NP; (2) that animals with SCI-NP showed higher spontaneous discharge rates compared to the other animal groups, particularly in the ventral horns; and (3) that animals with chronic SCI exhibited higher neuronal variability compared to neurologically intact animals. Together, the results suggest that increased SpAP in dorsal and ventral neurons may further exacerbate pathological sensory transmission after SCI and be a component of SCI-NP.