Gregory E. Morley, PhD

My current research interests are focused on determining the molecular mechanisms of initiation and maintenance of ventricular arrhythmias using normal and transgenic mice. Transmission of electrical current through gap junctions in the heart is essential for normal heart function. Disturbing the sequence of excitation either by altering the coupling between cells or by changing excitability compromises the ability of the heart to function efficiently. Changes in both excitability and intercellular communication are known to occur under a variety of pathological conditions, including acute myocardial ischemia, myocardial hypertrophy and atrial fibrillation. An imbalance in these parameters leads to the development of cardiac arrhythmias. Although numerous studies have sought to characterize the changes in active membrane currents, many important questions remain unanswered regarding the role of changes in intercellular communication. In the laboratory we employ state of the art imaging techniques to study electrical wave propagation at both the macroscopic and cellular level. In addition, we utilize newly developed quantitative methods to accurately define and measure patterns of wave propagation, conduction velocity and wave front curvature on the epicardial and endocardial surfaces of the adult, new born and embryonic mouse hearts. With this technology, we have been able to characterize normal and abnormal conduction patterns and have obtained the first high-resolution images of electrical wave propagation in mice lacking the gap junction proteins connexin40 (see figure) and connexin43. These studies promise to provide fundamental insight on the role of reduced intercellular coupling in the development of malignant cardiac arrhythmias.

The long range goals of our laboratory are to determine the fundamental mechanisms of impulse initiation and conduction and the role they play in triggering and maintaining cardiac arrhythmias.