Protein Tyrosine Phosphatase r Inhibitory Peptide Promotes Recovery of Diaphragm Function and Sprouting of Bulbospinal Respiratory Axons after Cervical Spinal Cord Injury

Damage to the respiratory neural circuitry after cervical spinal cord injury (SCI) can lead to diaphragm paralysis. The study investigates the use of a PTPr inhibitory peptide to promote axon plasticity and respiratory recovery in a rat model of C2 hemisection SCI. The PTPr peptide was applied locally to the injury site and surrounding spinal cord using a gelfoam release strategy. The study found that the PTPr peptide significantly improved ipsilateral hemidiaphragm function. The PTPr peptide stimulated robust sprouting of contralateral-originating rVRG fibers and serotonergic axons within the PhMN pool ipsilateral to hemisection. This suggests that the PTPr peptide-induced restoration of function was attributed to plasticity of spared axon pathways descending in contralateral spinal cord.

• 1
  PTPr peptide significantly improved ipsilateral hemidiaphragm function, as assessed in vivo with electromyography recordings.
• 2
  PTPr peptide stimulated robust sprouting of contralateral-originating rVRG fibers and serotonergic axons within the PhMN pool ipsilateral to hemisection.
• 3
  Relesion through the hemisection did not compromise diaphragm recovery, suggesting that PTPr peptide-induced restoration of function was attributed to plasticity of spared axon pathways descending in contralateral spinal cord.