V2a neurons restore diaphragm function in mice following spinal cord injury

Victoria N. Jensen, Emily E. Huffman, Frank L. Jalufka, Anna L. Pritchard, Sarah Baumgartner, Ian Walling, Holly C Gibbs, Dylan A. McCreedy, Warren J. Alilain, Steven A. Crone

Research output: Contribution to journalArticlepeer-review


The specific roles that different types of neurons play in recovery from injury is poorly understood. Here, we show that increasing the excitability of ipsilaterally projecting, excitatory V2a neurons using designer receptors exclusively activated by designer drugs (DREADDs) restores rhythmic bursting activity to a previously paralyzed diaphragm within hours, days, or weeks following a C2 hemisection injury. Further, decreasing the excitability of V2a neurons impairs tonic diaphragm activity after injury as well as activation of inspiratory activity by chemosensory stimulation, but does not impact breathing at rest in healthy animals. By examining the patterns of muscle activity produced by modulating the excitability of V2a neurons, we provide evidence that V2a neurons supply tonic drive to phrenic circuits rather than increase rhythmic inspiratory drive at the level of the brainstem. Our results demonstrate that the V2a class of neurons contribute to recovery of respiratory function following injury. We propose that altering V2a excitability is a potential strategy to prevent respiratory motor failure and promote recovery of breathing following spinal cord injury.

Original languageEnglish
Pages (from-to)e2313594121
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number11
StatePublished - Mar 12 2024


  • breathing
  • electromyography
  • neuroplasticity
  • spinal cord injury
  • V2a neuron

ASJC Scopus subject areas

  • General


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