期刊
JOURNAL OF PHYSIOLOGY-LONDON
卷 533, 期 1, 页码 185-199出版社
CAMBRIDGE UNIV PRESS
DOI: 10.1111/j.1469-7793.2001.0185b.x
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1.To examine whether a capacitative Ca2+ entry pathway is present in skeletal muscle, thin muscle fibre bundles were isolated fr om extensor digitorum longus (EDL) muscle of adult mice, and isometric tension and fura-2 signals were simultaneously measured. 2. The sarcoplasmic reticulum (SR) in the muscle fibres was successfully depleted of Ca2+ by repetitive treatments with high-K+ solutions, initially in the absence and then in the presence of a sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA) inhibitor. 3. Depletion of the SR of Ca2+ enabled us for the first time to show convincingly that the vast majority of the voltage-sensitive Ca2+ store overlaps the caffeine-sensitive Ca2+ store in intact fibres from mouse EDL muscle. This conclusion was based on the observation that both high-K+ solution and caffeine failed to cause a contracture in the depleted muscle fibres. 4. The existence of a Ca2+ influx pathway active enough to refill the depleted SR within several minutes was shown in skeletal muscle fibres. Ca2+ entry was sensitive to Ni2+, but resistant to nifedipine and was suppressed by plasma membrane depolarisation. 5. Evidence for store-operated Ca2+ entry was provided by measurements of Mn2+ entry. Significant acceleration of Mn2+ entry was observed only when the SR was severely depleted of Ca2+. The Mn2+ influx, which was blocked by Ni2+ but not by nifedipine, was inwardly rectifying as is the case with the Ca2+ entry. These results indicate that the store-operated Ca2+ entry is similar to the Ca2+ release-activated Ca2+ channel (CRAC) current described in other preparations.
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