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Gregory E. Morley, Ph.D.

Research in Dr. Morley’s laboratory is focused on determining the molecular mechanisms of initiation and maintenance of atrial and ventricular arrhythmias. Transmission of electrical current through gap junction channels is essential for normal heart function. Disturbing the sequence of excitation either by altering 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. An imbalance in these parameters can lead to the development of cardiac arrhythmias. 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 in the adult, new born and embryonic mouse hearts. These studies promise to provide fundamental insight into the role of reduced intercellular coupling in the development of malignant cardiac arrhythmias.

Selected Publications

  1. Tamaddon, H.S., Vaidya, D, Simon, A M., Paul, D.L., Jalife, J., Morley, G.E. High-resolution optical mapping of the right bundle branch in connexin40 knockout mice reveals slow conduction in the specialized conduction system. Circ.Res. 2000;87:929-93.
  2. Morley, G.E., Vaidya, D. Understanding conduction of electrical impulses in the mouse heart using high-resolution video imaging technology. Micro.Res.Tech. 2001;52:241-250.
  3. Gutstein, D. E., Morley, G. E., Tamaddon, H., Vaidya, D., Schneider, M. D., Chen, J., Chien, K. R., Stuhlmann, H., Fishman, G. I. Conduction Slowing and Sudden Arrhythmic Death in Mice With Cardiac-Restricted Inactivation of Connexin43. Circ. Res. 2001;88:333-339.
  4. Rentschler S., Tamaddon H., Degenhardt K., Sassoon D., Morley, G.E. Jalife, J., Fishman, G.I. Visualization of the Developing Murine Cardiac Conduction System by Engrailed-2 Development. 2001;128:1785-1792.
  5. Vaidya, D.M., Tamaddon, H.S., Lo, C.W., Taffet, S., Delmar, M., Morley, G.E., Jalife, J. Null Mutation of Connexin43 Causes Slow Propagation of Ventricular Activation in the Late Stages of Mouse Embryonic Development. Circ.Res. 2001;88:1196-1202.
  6. Sornborger, A., Sirovich, L. Morley, G.E. A method for denoising periodic multivariate signals: application to voltage dye imaging of the mouse heart. IEEE Medical Imaging. 2003;22:1537-49.
  7. Chuck, E.T., Meyers, K., France, D., Creazzo, T.L., Morley, G.E. Transitions in Ventricular Activation Revealed by Two-Dimensional Optical Mapping. Anat. Rec. 2004;280A:990-1000.
  8. Morley, G.E., Danik, S.B., Sun, Y., Rosner, G., Gutstein, D.E. Fishman, G.I. Modulation of Source-Sink Mismatch in the Heart Results in Paradoxical Purkinje-Ventricular Muscle Propagation and the Initiation of Lethal Arrhythmias. Proc. Natl. Acad. Sci. 2004 102(11):4126-9
  9. Gaussin, V., Morley, G.E., Cox, L., Tian, Y., Emile, L., Liu, J., Hong, C., Myers, D., Conway, S.J., Depre, C., Mishina, Y., Behringer, R.R., Hanks, M.C., Zwijsen, A., Huylebroeck, D., Fishman, G.I., Schneider, M.D., Burch, J.B., Vatner, S.F. Alk3/Bmpr1a receptor is required for development of the atrioventricular canal into valves and annulus fibrosus. 2005; Circ. Res. 97(3):219-26
  10. Li, J., Patel, V.V., Kostetskii, I., Xiong, Y., Chu, A.F., Jacobson, J.T., Yu, C., Morley, G.E., Molkentin, J.D., Radice, G.L. Cardiac-specific loss of N-cadherin leads to alteration in connexins with conduction slowing and arrhythmogenesis. 2005; Circ. Res. 97(5):474-81.
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