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1. Single Purkinje cells, enzymatically isolated from rabbit ventricle, were studied under whole-cell voltage clamp conditions and internally perfused with the fluorescent Ca2+ indicator fura-2(100 microM). 2. Ca2+ release from the sarcoplasmic reticulum was either induced by external application of caffeine or occurred spontaneously in Ca2+i-overloaded cells. Membrane currents accompanying these Ca(2+)-release signals were studied at steady membrane potentials. 3. [Ca2+]i transients were accompanied by transient membrane currents. In the absence of Na(+)-Ca2+ exchange, two current components could be observed. The first component peaked well before the [Ca2+]i transient (Ifast) and relaxed before peak [Ca2+]i. The second component, on the other hand, peaked at the time when [Ca2+]i was maximal (Islow). 4. In symmetrical Cl- solutions both current components had a reversal potential close to O mV. A reduction of external or internal [Cl-] shifted this reversal potential in accordance with the change of the Cl- equilibrium potential. 5. Each [Ca2+]i transient was accompanied by Ifast. Properties of Ifast suggest that this current component is the [Ca2+]i-dependent Cl- current, ICl(Ca), previously observed during depolarizing pulses. 6. Islow was only detected in cells that displayed a large [Ca2+]i transient with or without elevated resting [Ca2+]i. 7. It is concluded that during large [Ca2+]i transients a slow component of ICl(Ca) can be activated. This second component may arise from the same channel population as the previously described fast component and be related to the presence of spatial and temporal inhomogeneities of [Ca2+]i. Alternatively, this current component may arise from a different Cl- channel population with a different Ca2+ sensitivity.
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