Abstract
Dihydropyridine-sensitive Ca 2+ channels in heart demonstrate an important negative feedback property: they close, or inactivate, in response to prior Ca 2+ entry. We now find that Ca 2+ influx through one channel can selectively contribute to the inactivation of another adjacent channel, without a generalized elevation of bulk intracellular Ca 2+ concentration. Intracellular application of the Ca 2+ chelator BAPTA greatly diminishes such negative interactions within Ca 2+ channel pairs. These findings demonstrate that Ca 2+ currents are controlled not only by intrinsic channel properties, but also by local diffusive interactions among neighboring channels. Such inhibitory coupling among channels provides a concrete example of localized Ca 2+ signaling, long proposed to exist on the basis of theoretical calculations.
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