H-reflex disinhibition by lumbar muscle inflammation in a mouse model of spinal cord injury.

Inflammation is a common comorbidity in patients with traumatic spinal cord injury (SCI). Recent reports indicate that inflammation hinders functional recovery in animal models of SCI. However, the spinal mechanisms underlying this alteration are currently unknown. Considering that spinal plasticity is a therapeutic target in patients and animal models of SCI, these mechanisms remain to be clarified. Using injections of complete Freund's adjuvant (CFA) in lumbar muscles as a model of persistent inflammation, the objective of this study was to assess the impact of inflammation on spinal reflex excitability after a complete midthoracic spinal transection in mice. To this end, the excitability of spinal reflexes was examined by measuring H-reflex frequency-dependent depression (FDD) on days 7, 14 and 28 following a complete spinal transection. H-reflex parameters were compared between spinal mice with CFA and control spinal mice. On day 7, lumbar muscle inflammation disinhibited the H-reflex, reflected by an attenuation of H-reflex FDD (p < 0.01), although this effect did not persist later on, either on day 14 or day 28. These results indicate that lumbar muscle inflammation alters spinal reflex excitability transiently in spinal mice. Considering that changes in spinal reflex excitability are associated with poor functional recovery after SCI, this implies that inflammation should be treated effectively to promote optimal recovery following SCI.