Diaphragm and intercostal neuromuscular plasticity following C2 spinal hemisection injury (C2HS)

Abstract

C2HS transiently paralyzes the ipsilateral (IL) hemidiaphragm (HD) and induces compensatory increases in contralateral (CL) HD activity. In ongoing experiments, we are examining how chronic C2HS in adult male Sprague‐Dawley rats influences CL HD fiber size and type, and the expression of myogenic markers. Parallel experiments are quantifying the impact of chronic C2HS on inspiratory intercostal muscle electromyogram (EMG) activity. Bilateral EMG recordings from the IL and CL HD (medial costal portion) and external intercostal muscles (5th space) were obtained in urethane‐anesthetized spontaneously breathing rats at 1–60 days post‐C2HS. Diaphragm tissue was then harvested and prepared for histological and immunohistochemical evaluation. Preliminary histological analyses indicated an increase in centrally located myonuclei in CL HD myofibers and inflammatory cell infiltration by 24 hrs post‐injury. In addition, there appears to be a reduction in the relative number of type 1 myofibers in the CL HD by 48 hours post‐injury. Robust inspiratory bursting was observed in the CL intercostal EMG of all rats. IL intercostal EMG bursting was evident as early as 24 hrs post‐C2HS, whereas IL HD EMG activity was absent even as late as 14 days post‐C2HS. We conclude that the CL diaphragm begins to remodel almost immediately following C2HS, and cross spinal pathways enable IL intercostal recovery shortly after injury.Support: NIH 1R01HD052682‐01A1, NIH T32 HD043730