Abstract.
The effects of long-term depolarization on the level of α1s and on L-type Ca2+ currents of skeletal muscle were investigated. Long-term depolarization (14 h) caused a 50% decrease of α1s, revealed with the Western blot technique. This decline was prevented by preincubation with the Ca2+ channel blocker nifedipine. Electrophysiological experiments using the voltage-clamp technique were performed to measure the actions of long-term depolarization on Ca2+ currents and charge movement. A progressive decline in the amplitude of the Ca2+ currents by depolarizations lasting 0.5–14 h was observed. Similar to Western blot results, the fall in current amplitude was prevented by nifedipine, and it depended on external Ca2+. The nonlinear charge mobilized by step pulses was also significantly reduced (50%) by long-term depolarization. It is suggested that α1s subunit is down-regulated by long-term depolarization by a very stringent mechanism and that, in this process, Ca2+ ions permeating through L-type channels play a key role. A new role for the L-type Ca2+ current in skeletal muscle fibers in which the channels are self-regulated is proposed.
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Escamilla, J., Farías, J.M., García, R. et al. Long-term depolarization regulates the α1s subunit of skeletal muscle Ca2+ channels and the amplitude of L-type Ca2+ currents. Pflügers Arch - Eur J Physiol 442, 882–890 (2001). https://doi.org/10.1007/s004240100606
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DOI: https://doi.org/10.1007/s004240100606