期刊论文详细信息
| FEBS Letters | |
| Involvement of Mg2+ in terminating Ca2+ release in cultured rat skeletal muscle | |
| Suda, Norio1  | |
| [1] Max-Planck-Institut für Biophysikalische Chemie, Am Fassberg 37077 Göttingen, Germany | |
| 关键词: Skeletal muscle; Excitation-contraction coupling; Ryanodine receptor; Ca2+ release channel; Caffeine; Fura-2; SR; sarcoplasmic reticulum; T-tubule; transverse tubule; RyR; ryanodine receptor; RISC; repolarization-induced stop of caffeine-induced Ca2+ release; DHPR; dihydropyridine receptor; TTX; tetrodotoxin; EGTA; ethylene-glycol-bis-N; N; N′; N′ tetraacetic acid; HEPES; N-2-hydroxyethyl-piperazine-N′-2-ethansulphonic acid; | |
| DOI : 10.1016/0014-5793(95)00047-D | |
| 学科分类:生物化学/生物物理 | |
| 来源: John Wiley & Sons Ltd. | |
PDF
|
|
【 摘 要 】
Combined patch-clamp and fura-2 measurements were performed to investigate the mechanism that terminates Ca2+ release in rat skeletal myoballs. When cells were intracellularly perfused with solution containing 1 mM free Mg2+, the caffeine (10 mM)-induced Ca2+ transient was abruptly terminated by membrane repolarization (−70 mV). With low intracellular Mg2+ (e.g. 50 μM) perfusion, however, repolarization failed to terminate the caffeine transient. The results show that intracellular Mg2+ is necessary for repolarization-induced closing of the Ca2+ release channel.
【 授权许可】
Unknown
【 预 览 】
| Files | Size | Format | View |
|---|---|---|---|
| RO201912020300691ZK.pdf | 624KB |
PDF