Background: The cellular basis for the monophasic action potential (MAP) has long been a matter of debate. At the center of the controversy is the issue as to which of the two electrodes is the recording electrode and which is the indifferent electrode. The present study is designed to address this issue. Methods: Transmembrane action potentials (TAPs) and either intramural MAPs or contact (Franz-like) MAPs were recorded from adjacent sites in canine arterially perfused ventricular wedge preparations. Intramural MAPs were recorded using thin wire electrodes referenced to a KCl electrode. Results: Local cooling or injection of ATX-II into the region subtending the inactivating (contact or KCl) electrode did not affect the MAP. Similar maneuvers at the site of the noninactivating electrode always prolonged the MAP. The intramural MAP always prolonged in proportion to the TAP, whereas the contact MAP did not, often displaying apparent early afterdepolarizations (EADs) or delayed afterdepolarizations (DADs) due to its much wider field of view, which captured activity from the region of prolonged repolarization as well as the remote normal regions. Conclusions: Our results suggest that (1) it is not the contact or MAP electrode that records the MAP, but rather the noninactivating “indifferent” electrode and (2) intramural MAPs provide more accurate recordings of local activity. The data provide compelling evidence in support of the hypothesis that the MAP represents the extracellular potential difference between active and inactive sites within the heart rather than injury currents flowing at the boundary of the active and inactive zone under the inactivating electrode.