Respiratory motor recovery after unilateral spinal cord injury: eliminating crossed phrenic activity decreases tidal volume and increases contralateral respiratory motor output.
By 2 months after unilateral cervical spinal cord injury (SCI), respiratory motor output resumes in the previously quiescent phrenic nerve. This activity is derived from bulbospinal pathways that cross the spinal midline caudal to the lesion (crossed phrenic pathways). To determine whether crossed phrenic pathways contribute to tidal volume in spinally injured rats, spontaneous breathing was measured in anesthetized C2 hemisected rats at 2 months after injury with an intact ipsilateral phrenic nerve, or with ipsilateral phrenicotomy performed at the time of the SCI (i.e., crossed phrenic pathways rendered ineffective) (dual injury). Ipsilateral phrenicotomy did not alter the rapid shallow eupneic breathing pattern in C2 injured rats. However, the ability to generate large inspiratory volumes after either vagotomy or during augmented breaths was impaired if crossed phrenic activity was abolished. We also investigated whether compensatory plasticity in contralateral motoneurons would be affected by eliminating crossed phrenic activity. Thus, contralateral phrenic motor output was recorded in anesthetized, vagotomized, and mechanically ventilated rats with dual injury during chemoreceptor stimulation. Hypercapnia, hypoxia, and asphyxia increased contralateral phrenic burst amplitude in the dual injury group more than in rats with SCI alone. Dual injury rats also had elevated baseline burst frequency. Together, these results demonstrate a functional role of crossed phrenic activity after SCI. Moreover, by preventing ipsilateral phrenic motor recovery in rats with unilateral SCI, segmental and supraspinal changes could be induced in contralateral respiratory motor output beyond that seen with SCI alone.
Golder
Francis J
FJ
Department of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville, Florida 32610, USA. golderf@svm.vetmed.wisc.edu
Fuller
David D
DD
Davenport
Paul W
PW
Johnson
Richard D
RD
Reier
Paul J
PJ
Bolser
Donald C
DC
D000818:Animals; D001237:Asphyxia / Q000503:physiopathology; D001784:Blood Gas Analysis; D001794:Blood Pressure; D002628:Chemoreceptor Cells / Q000502:physiology; D003714:Denervation; D004594:Electrophysiology; D005260:Female; D007839:Functional Laterality; D006935:Hypercapnia / Q000503:physiopathology; D018496:Hyperoxia / Q000503:physiopathology; D000860:Hypoxia / Q000503:physiopathology; D009046:Motor Neurons / Q000502:physiology; D009333:Neck; D009473:Neuronal Plasticity; D010791:Phrenic Nerve / Q000502:physiology / Q000503:physiopathology*; D051381:Rats; D020127:Recovery of Function / Q000502:physiology; D012132:Respiratory Muscles / Q000294:innervation / Q000503:physiopathology; D012133:Respiratory Paralysis / Q000209:etiology / Q000503:physiopathology*; D013047:Specific Pathogen-Free Organisms; D013119:Spinal Cord Injuries / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D013990:Tidal Volume; D014628:Vagotomy