Hypoxia triggers short term potentiation of phrenic motoneuron discharge after chronic cervical spinal cord injury

Kun Ze Lee, Milapjit S. Sandhu, Brendan J. Dougherty, Paul J. Reier, David D. Fuller

Research output: Contribution to journalArticlepeer-review

22 Scopus citations


Repeated exposure to hypoxia can induce spinal neuroplasticity as well as respiratory and somatic motor recovery after spinal cord injury (SCI). The purpose of the present study was twofold: to define the capacity for a single bout of hypoxia to trigger short-term plasticity in phrenic output after cervical SCI and to determine the phrenic motoneuron (PhrMN) bursting and recruitment patterns underlying the response. Hypoxia-induced short term potentiation (STP) of phrenic motor output was quantified in anesthetized rats 11weeks following lateral spinal cord hemisection at C2 (C2Hx). A 3-min hypoxic episode (12-14% O2) always triggered STP of inspiratory burst amplitude, the magnitude of which was greater in phrenic bursting ipsilateral vs. contralateral to C2Hx. We next determined if STP could be evoked in recruited (silent) PhrMNs ipsilateral to C2Hx. Individual PhrMN action potentials were recorded during and following hypoxia using a "single fiber" approach. STP of bursting activity did not occur in cells initiating bursting at inspiratory onset, but was robust in recruited PhrMNs as well as previously active cells initiating bursting later in the inspiratory effort. We conclude that following chronic C2Hx, a single bout of hypoxia triggers recruitment of PhrMNs in the ipsilateral spinal cord with bursting that persists beyond the hypoxic exposure. The results provide further support for the use of short bouts of hypoxia as a neurorehabilitative training modality following SCI.

Original languageEnglish (US)
Pages (from-to)314-324
Number of pages11
JournalExperimental Neurology
StatePublished - Jan 1 2015
Externally publishedYes

Bibliographical note

Funding Information:
Support for this work was provided by grants from the National Institutes of Health (NIH): NIH 1R01NS080180-01A1 (DDF) and 1R01NS054025-06 (PJR) and a grant from the State of Florida Brain and Spinal Cord Injury Research Program (DDF and PJR) administered through the McKnight Brain Institute at the University of Florida. KZL was partially supported by grants from the National Science Council Taiwan (NSC 102-2320-B-110-004-MY3 ), National Health Research Institutes ( NHRI-EX103-10223NC ), NSYSU–KMU Joint Research Project ( 2014-I006 ) and the Paralyzed Veterans of America Research Foundation (grant # 2691 ). MS was supported by the Craig H. Neilsen Foundation (grant # 220521 ).

Publisher Copyright:
© 2014 Elsevier Inc.


  • Hypoxia
  • Neuroplasticity
  • Phrenic
  • Recruitment
  • Spinal cord injury


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