ABSTRACT
Years elapsed before the discovery of corresponding behavior within vertebrate and mammalian systems, which awaited technological renements enabling routine isolation and voltage clamp of Ca2+ currents in cells from these organisms. Among other systems, a urry of reports then arose in cardiac muscle regarding the existence of CDI in L-type Ca2+ currents of the heart (carried by Ca V1.2 channels); this story was revealed in preparations extending from the multicellular context (Kass and Sanguinetti 1984; Mentrard et al. 1984) to the level of isolated single cells (Lee et al. 1985). As an illustration, Figure 35.1a (Ca) shows Ca2+ current from frog myocytes, as evoked by a test voltage pulse to ER + 80 mV (Mentrard et al. 1984). e actual extent of Ca2+ current (shaded area) was gauged by cobalt blockade of Ca2+ current (Co). To characterize CDI, Ca2+ entry during a prepulse of voltage to ER + 80 mV (Figure 35.1b) can be seen to inactivate Ca2+ current in a closely ensuing test pulse (diminished area of shading). To distinguish this inactivation from that produced simply by voltage depolarization, a prepulse to ER + 120 mV
(Figure 35.1c) can be observed to produce far less inactivation in a subsequent test-pulse current. Because this prepulse entails strong depolarization, but decreased Ca2+ entry from attenuated Ca2+ entry driving force, the restoration of test Ca2+ current here argues that the potent inactivation in Figure 35.1b could be attributed to CDI. Data such as these reveal an inactivation process that depends upon voltage as a U-shaped function, now considered one hallmark of CDI (Eckert and Tillotson 1981).
