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小鼠骨骼肌纤维去极化诱导细胞内钙离子增加从而激活钙激活钾通道。

Activation of Ca2+-activated K+ channels by an increase in intracellular Ca2+ induced by depolarization of mouse skeletal muscle fibres.

作者信息

Jacquemond V, Allard B

机构信息

Laboratoire de Physiologie des Elements Excitables, CNRS UMR 5578, Universite Claude Bernard Lyon 1, 43 boulevard du 11 Novembre 1918, 69622 Villeurbanne Cedex, France.

出版信息

J Physiol. 1998 May 15;509 ( Pt 1)(Pt 1):93-102. doi: 10.1111/j.1469-7793.1998.093bo.x.

Abstract
  1. Ionic currents were simultaneously recorded at macroscopic and unitary level using the whole-cell and cell-attached patch-clamp procedures together on the same portion of isolated mouse skeletal muscle fibres. 2. In the presence of Tyrode solution in the patch pipette and Tyrode-TTX solution in the bath, macroscopic and unitary currents through delayed rectifier K+ channels were simultaneously recorded in response to depolarizing pulses of 1 s duration. 3. In five fibres, successive long-lasting incremental depolarizing levels induced, at -40 mV or -30 mV, the opening of a high conductance channel carrying an outward current superimposed on delayed rectifier K+ channel activity. Opening of this high conductance channel was not observed when the depolarization steps were applied in the patch pipette. 4. Using the same depolarizing protocol, activation of a high conductance channel was also observed in two fibres in the presence of a K+-rich solution in the pipette (145 mM K+) . 5. With either Tyrode or K+-rich solution in the pipette, unitary current amplitudes of the high conductance channel matched well with the values obtained for Ca2+-activated K+ (KCa) channels in inside-out patches under similar ionic conditions. 6. Indo-1 fluorescence measurements showed that the stimulation protocol that led to KCa channel opening induced stepwise increases in intracellular [Ca2+] in the submicromolar range. 7. Our results provide evidence that activation of sarcolemmal KCa channels can be induced by a rise in intracellular [Ca2+] following voltage-activated sarcoplasmic reticulum Ca2+ release.
摘要
  1. 使用全细胞和细胞贴附式膜片钳技术,在分离的小鼠骨骼肌纤维的同一部分同时记录宏观和单位水平的离子电流。2. 在膜片电极中加入台氏液且浴槽中加入台氏 - 河豚毒素溶液的情况下,响应持续1秒的去极化脉冲,同时记录通过延迟整流钾通道的宏观电流和单位电流。3. 在五根纤维中,在 -40 mV或 -30 mV时,连续的长时间递增去极化水平诱导了一个高电导通道的开放,该通道携带外向电流,叠加在延迟整流钾通道活性之上。当在膜片电极中施加去极化步骤时,未观察到该高电导通道的开放。4. 使用相同的去极化方案,在膜片电极中存在富含钾的溶液(145 mM K+)的情况下,在两根纤维中也观察到了高电导通道的激活。5. 无论膜片电极中是台氏液还是富含钾的溶液,高电导通道的单位电流幅度与在类似离子条件下内面向外膜片中钙激活钾(KCa)通道获得的值匹配良好。6. Indo - 1荧光测量表明,导致KCa通道开放的刺激方案在亚微摩尔范围内诱导细胞内[Ca2+]逐步增加。7. 我们的结果提供了证据,表明电压激活的肌浆网Ca2+释放后细胞内[Ca2+]的升高可诱导肌膜KCa通道的激活。

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本文引用的文献

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Potassium contractures in single muscle fibres.单根肌纤维中的钾挛缩
J Physiol. 1960 Sep;153(2):386-403. doi: 10.1113/jphysiol.1960.sp006541.

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