Cervical excitatory neurons sustain breathing after spinal cord injury

Kajana Satkunendrarajah (), Spyridon K. Karadimas, Alex M. Laliberte, Gaspard Montandon and Michael G. Fehlings ()
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Kajana Satkunendrarajah: University Health Network
Spyridon K. Karadimas: University of Toronto
Alex M. Laliberte: University Health Network
Gaspard Montandon: St Michael’s Hospital
Michael G. Fehlings: University Health Network

Nature, 2018, vol. 562, issue 7727, 419-422

Abstract: Abstract Dysfunctional breathing is the main cause of morbidity and mortality after traumatic injury of the cervical spinal cord1,2 and often necessitates assisted ventilation, thus stressing the need to develop strategies to restore breathing. Cervical interneurons that form synapses on phrenic motor neurons, which control the main inspiratory muscle, can modulate phrenic motor output and diaphragmatic function3–5. Here, using a combination of pharmacogenetics and respiratory physiology assays in different models of spinal cord injury, we show that mid-cervical excitatory interneurons are essential for the maintenance of breathing in mice with non-traumatic cervical spinal cord injury, and are also crucial for promoting respiratory recovery after traumatic spinal cord injury. Although these interneurons are not necessary for breathing under normal conditions, their stimulation in non-injured animals enhances inspiratory amplitude. Immediately after spinal cord injury, pharmacogenetic stimulation of cervical excitatory interneurons restores respiratory motor function. Overall, our results demonstrate a strategy to restore breathing after central nervous system trauma by targeting a neuronal subpopulation.

Keywords: Inspiratory Amplitude; Cervical Interneurons; Phrenic Motoneurons; Vesicular Glutamate Transporter (VGLUT2); Designer Receptors Exclusively Activated By Designer Drugs (DREADD) (search for similar items in EconPapers)
Date: 2018
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DOI: 10.1038/s41586-018-0595-z

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