Most spinal cord injuries (SCI) involve the cervical level and result in respiratory complications due to impaired diaphragm activation. The diaphragm (main inspiratory muscle) is composed of different types of motor units that generate varying amounts of force and accomplish a range of motor behaviors. There are considerable differences in the intrinsic properties of phrenic motor neurons and the motor units they comprise. Our laboratory has long explored mechanisms underlying recruitment of diaphragm motor units to accomplish lower force ventilatory (e.g., eupnea, hypoxia-hypercapnia) behaviors that recruit small phrenic motor neurons, and higher force airway clearance behaviors (e.g., airway occlusion, coughing, and sneezing) that recruit large phrenic motor neurons. In recent studies, we found that there is a differential impact of an incomplete SCI on diaphragm activity, such that, only lower force ventilatory behaviors are impacted. Converging evidence also strongly supports the role of BDNF/TrkB and NMDA mediated glutamatergic signalling in the neuroplasticity that underlies spontaneous recovery of diaphragm activity following injury. Recognizing the importance of considering motor neuron size in the recruitment of motor units, we employ single cell multiplex fluorescence in situ hybridization to explore the heterogeneity of TrkB and glutamatergic receptor mRNA expression across phrenic motor neurons in a sized dependent fashion. These studies provide first of its kind information about neuroplasticity within a motor pool and the effect on a range of behaviors important for both ventilation and maintenance of airway clearance.
This webcast will discuss:
- Is there heterogeneity in motor neuron properties within a motor neuron pool and how does this contribute to neuromotor control?
- How can we use single cell RNAscope in situ technology to assess neuronal activation patterns in response to injury?
- How to evaluate cellular mechanisms of neuroplasticity using RNAscope in situ technology.
