Gonoi T, Hasegawa S
Research Center for Pathogenic Fungi and Microbial Toxicoses, Chiba University, Japan.
Pflugers Arch. 1991 Dec;419(6):657-61. doi: 10.1007/BF00370311.
The whole-cell voltage-clamp technique was used to study the physicochemical nature and regulatory mechanisms of inward rectifier K+ currents in skeletal muscle fibres (flexor digitorum brevis muscle) of newborn mice. The inward rectifier K+ currents were at hardly discernible levels (less than or equal to 15 microA/cm2) in fibres acutely isolated from 1-day-old (P1) mice or P1 fibres cultured without any added reagents for 1-3 days. When A23187 (1 microM), ionomycin (3 microM) or ryanodine (greater than or equal to 0.03 microM) was added to a culture medium, a significant increase of the inward rectifier current (-106 +/- 46 microA/cm2 at a membrane potential of -100 mV and an extracellular K+ concentration of 20 mM for the case of A23187) was observed within 1 day after the addition of the reagents. The inward rectifier current decreased to the level of control cultures within 11 h after a removal of A23187. The increase of the current with A23187 was inhibited with actinomycin D, cycloheximide or colchicine, but not with tunicamycin or cytochalasin B. We suggest that the functional inward rectifiers are induced in skeletal muscle fibres by elevation of the cytosolic Ca2+ concentration in a transcription and protein synthesis dependent manner and that the microtubular system is necessary for this induction.
