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Much of my earlier scientific work concerned the characterization of Ca2+ currents and Ca2+ transport in heart cells. After my initial discovery of a Ca2+ current in heart cells in 1967, I characterized the relevance of this current for excitation and excitation-contraction coupling in cardiac muscle. My colleagues and I demonstrated the importance of the Ca2+ current during the plateau phase of the cardiac action potential for the filling of intracellular Ca2+ stores. This is an essential mechanism involved in contraction of the heart. We also found that catecholamines greatly enhance the Ca2+ current and that cAMP analogues mimic the effect of catecholamines. This was probably the first demonstration of modulation of a voltage-gated ion channel. More recently, molecular mechanisms involved in voltage- and Ca2+ dependent inactivation and in dihydropyridine binding in mutants of human L-type Ca2+ channels are being studied. In 1968, we described the Na-Ca exchanger as a transport mechanism capable of extruding Ca2+ out of cardiac cells against a large electrochemical gradient. Our current studies deal with the localization of the exchanger and other Ca2+-transport systems in single presynaptic boutons of hippocampal cells. This is relevant for our understanding of the kinetics of vesicle cycling and neurotransmitter release.
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Physiology Newspp.32-37, (2014)
Natureno. 6641 (1997): 478-482
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