Spinal cord injury is devastating, not only because it causes paralysis but because it disrupts the regulation of the circulation. Spinally injured patients can experience extreme, life-threatening increases in arterial pressure. As the likelihood of therapeutic spinal cord regeneration increases, so does the concern that, if regenerating pathways do not make appropriate connections, equally serious autonomic dysfunction could result. We study the spinal systems that affect arterial pressure before and after spinal injury. Our goal in identifying and understanding these systems is to predict potential cardiovascular dysfunction in the event of inappropriate regeneration of pathways during spinal cord regeneration.

What tools do we use? Engineering plays two important roles in our research. First, the acquisition and analysis of signals from single and multiple neurons requires a range of techniques that are drawn largely from electrical engineering. These include high speed data acquisition from multiple neurons and on- and offline processing of these signals in both time and frequency domains. Second, we develop computational models of the neural systems that we hypothesize are responsible for the behavior we observe in spinal cord autonomic systems. These models are used both to test the validity of current models and to develop our next generation of hypotheses. The laboratory also uses many non-engineering methods. These include immunohistochemical identification of putative neuronal transmitters, juxtacellular labeling of neurons, and retrograde and anterograde tracing of neuronal pathways using both dyes and viruses.

What's an example of one of our discoveries? We have developed both physiological and anatomical methods that identify populations of spinal neurons that are responsible for generating activity in the sympathetic nervous system after spinal cord injury. Using this method, we have shown recently that after chronic transection circuits in the spinal cord become much more sensitive to even innocuous mechanical stimulation of the skin. This discovery, predicts the kinds of autonomic dysfunction that might occur if, during recovery from spinal cord injury, regenerating neural pathways do not establish appropriate connections.