Robert Harvey Ph.D.: Biography/Education


Cellular and Molecular Pharmacology & Physiology | COBRE in Cell Biology | Department of Pharmacology


  • Ph.D. Pharmacology, Northwestern, 1987
  • B.S. Pharmacy, Drake University, 1982


Sudden cardiac death kills as many as 300,000 Americans every year, and in most cases the ultimate demise of the individual is due to the abrupt onset of abnormal electrical activity or cardiac arrhythmia. Even though the incidence of sudden cardiac death is often associated with some sort of preexisting condition, a significant number of victims have no apparent underlying cardiovascular disease. The critical, yet unanswered question is what triggers fatal arrhythmias in these individuals? Although the mechanisms responsible remain largely unknown, there is substantial evidence that heart-brain interactions involving the autonomic nervous system play a critical role in many cases. Our working hypothesis is that dynamic interactions between the sympathetic and parasympathetic branches of the autonomic nervous system trigger abnormal electrical responses that can lead to the generation of life threatening ventricular arrhythmias. We believe that these abnormal responses are due to complex subcellular signaling mechanisms that affect the activity of a number of different ion channels in the heart. To test our hypothesis, we are using a systems biology approach that combines computational modeling with a variety of powerful experimental techniques. These include single cell recording of membrane currents and action potentials as well as live cell imaging of subcellular signaling responses using fluorescence resonance energy transfer (FRET) based biosensors. The ultimate goal is to identify the conditions under which imbalances in autonomic tone are likely to trigger ventricular arrhythmias in order that they might be prevented.

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