ABSTRACT

Chimeras consisting of the homologous skeletal dihydropyridine receptor (DHPR) [beta]1a subunit and the heterologous cardiac/brain [beta]2a subunit were used to determine which regions of [beta]1a were responsible for the skeletal-type excitation-contraction (EC) coupling phenotype. Chimeras were transiently transfected in [beta]1 knockout myotubes and then voltage-clamped with simultaneous measurement of confocal fluo-4 fluorescence. All chimeras expressed a similar density of DHPR charge movements, indicating that the membrane density of DHPR voltage sensors was not a confounding ...

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