Our research focuses on neuromotor control of the diaphragm muscle during breathing. Phrenic motor neurons innervating diaphragm muscle fibers receive descending excitatory input from the brainstem, which is primarily ipsilateral and therefore disrupted by upper cervical spinal cord hemisection or C2SH. Following C2SH, there is spontaneous recovery of ipsilateral diaphragm activity reflecting neuroplasticity.
A major development is demonstrating a role of brain-derived neurotropic factor or BDNF signaling through its high affinity TrkB receptor in the recovery of diaphragm activity following C2SH. A second development is the use of machine learning approaches to facilitate high throughput analyses of diaphragm activity during numerous respiratory cycles. The lack of reliable, unbiased high throughput techniques to evaluate basic elements of diaphragm neuromotor control is a challenge in defining recovery of function.
This becomes especially important when you're dealing with recordings from animals that are not anesthetized. Our cervical spinal hemisection intentionally leaves the ipsilateral dorsal funiculus intact, minimizing limb muscle deficits, but still causing loss of diaphragm activity. This protocol emphasizes validation of the loss of diaphragm activity at the time of surgery, thereby establishing a clear starting point for recovery of diaphragm muscle function.
Further exploring the role of BDNF TrkB signaling in neuroplasticity and recovery of diaphragm neuromotor control after cervical spinal cord injury.
