Abstract

Anatomical data from our laboratory indicate that phrenic afferent fibers can project across the spinal midline and neurophysiological data indicate that electrical activation of phrenic afferents can increase contralateral phrenic motor output. We have also observed that following chronic unilateral C2 hemisection (C2Hx) phrenic nerve afferent fibers undergo significant anatomical remodeling. Here we tested the hypothesis that following chronic C2Hx, activation of ipsilateral (same side as injury) phrenic afferent neurons would induce contralateral (opposite to injury) phrenic motor plasticity. Twelve weeks after unilateral C2Hx (n=9) or C2 laminectomy (n=8), adult Sprague‐Dawley rats were anesthetized, vagotomized, and ventilated to enable phrenic motor output to be studied under controlled conditions. The phrenic nerve ipsilateral to C2Hx or laminectomy was electrically stimulated using a bipolar electrode while contralateral phrenic motor output was recorded. Rats received 30 minutes of inspiratory triggered stimulation (90μA, 40pps, 1ms pulse width) and contralateral phrenic motor output was recorded for one hour. Analysis of contralateral burst amplitude using a two‐way repeated measures ANOVA revealed a significant effect of time (F3,45=9.505, P<0.0001), but not treatment (C2Hx vs. laminectomy, F1,15=0.1577, P=0.6969). Thus, phrenic burst amplitude was significantly changing over the 60 minute post‐stimulation, and both experimental groups had increased phrenic burst amplitude during this period (P<0.05 vs. pre‐stimulation baseline). These results indicate that electrical activation of phrenic nerve afferent fibers can induce a sustained increased (facilitation) of contralateral phrenic motor output after spinal cord injury. The response was not statistically different in the laminectomy group, which indicates that the phrenic afferent‐induced facilitation does not require conditions induced by the spinal cord injury. The ability of phrenic afferent neurons to evoke phrenic motor plasticity after spinal cord injury suggests that these afferent pathways could be important to rehabilitation of the diaphragm motor system post‐injury.Support or Funding InformationK99HL143207‐01 (KS), F32NS095620‐01 (KS), T32HL134621‐01A1 (LBW), SPARC OT2 OD023854 (DDF)This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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