Harnessing sensorimotor circuit plasticity to maximize locomotor recovery after spinal cord injury

Spinal cord injury instantaneously and dramatically alters a person’s life. With interruption of nerve signals from the brain to the spinal cord, patients often face lasting motor dysfunctions. Scientific effort to date shows that electrical stimulation of the spinal cord below injury is one of promising methods to compensate for the loss of brain signals. To optimize such methods, we need to understand which cell types in the spinal cord are responsible for different types of motor functions. Moreover, we need to understand how much the spinal cord can learn to walk again with little help from the brain and which cell types are accountable for motor improvements. To address these questions, we use the mouse model to study a specific nerve cell-type using genetic techniques. We combine advanced virus-mediated technologies to visualize cell-to-cell connections and to manipulate cell functions while spinal cord injured mice are walking. Here, we ask two main questions: 1. Which cells in the spinal cord are responsible for learning to walk again without brain signals? And how do nerve cells function differently in spinal cords severely injured as juvenile or adult? 2. How does sensory input to the spinal cord maximize motor recovery? Studies with mouse models are essential and irreplaceable to provide a logical base and to advance the efficacy of future therapeutic interventions, especially in the field of neurorehabilitation using locomotor training and electrical stimulation.