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首页> 外文期刊>The Journal of Physiology >Veratridine-induced oscillations of cytosolic calcium and membrane potential in bovine chromaffin cells.
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Veratridine-induced oscillations of cytosolic calcium and membrane potential in bovine chromaffin cells.

机译：Veratridine诱导的牛嗜铬细胞胞质钙和膜电位的振荡。

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1. Veratridine (VTD) induced large oscillations of the cytosolic Ca2+ concentration ([Ca2+]i) and the membrane potential (Vm) in otherwise silent bovine chromaffin cells loaded with fura-2. 2. Depletion of the intracellular Ca2+ stores by thapsigargin or ryanodine did not affect these oscillations. Caffeine had a complex effect, decreasing them in cells with high activity but increasing them in cells with low activity. 3. The [Ca2+]i oscillations required extracellular Ca2+ and Na+ and were blocked by Ni2+ or tetrodotoxin. They were antagonized by high external concentrations of Mg2+ and/or Ca2+. 4. The oscillations of Vm had three phases: (i) slow depolarization (20 mV in 10-40 s); (ii) further fast depolarization (30 mV in 1 s); and (iii) rapid (5 s) repolarization. [Ca2+]i decreased during (i), increased quickly during (ii) with a 1 s delay with regard to the peak depolarization, and decreased during (iii). 5. Slight depolarizations increased the frequency of the oscillations whereas large depolarizations decreased it. 6. The Ca(2+)-dependent K+ channel blocker apamin increased the duration and decreased the frequency of the oscillations. 7. We propose the following mechanism for the oscillations: (i) the membrane depolarizes slowly by a decrease of potassium conductance (gK), perhaps due to a gradual decrease of [Ca2+]i; (ii) the threshold for activation of Na+ channels (decreased by VTD) is reached, producing further depolarization and recruiting Ca2+ channels, and inactivation of both Ca2+ and VTD-poisoned Na+ channels is slow; and (iii) gK increases, aided by activation of Ca(2+)-dependent K+ channels by the increased [Ca2+]i, and the membrane repolarizes. The contribution of the Na+ channels seems essential for the generation of the oscillations. 8. Bovine chromaffin cells have the machinery required for [Ca2+]i oscillations even though the more physiological stimulus tested here (high K+, field electrical stimulation, nicotinic or muscarinic agonists) produced mainly non-oscillatory responses.
机译：1.在装有fura-2的沉默牛嗜铬细胞中，维拉替丁（VTD）引起胞浆Ca2 +浓度（[Ca2 +] i）和膜电位（Vm）的大幅振荡。 2. thapsigargin或ryanodine耗尽了细胞内Ca2 +的储存量不会影响这些振荡。咖啡因具有复杂的作用，在具有高活性的细胞中降低它们，但在具有低活性的细胞中增加它们。 3. [Ca2 +] i振荡需要细胞外Ca2 +和Na +，并被Ni2 +或河豚毒素所阻断。它们被外部高浓度的Mg2 +和/或Ca2 +所拮抗。 4. Vm的振荡分为三个阶段：（i）缓慢去极化（10-40 s内为20 mV）; （ii）进一步快速去极化（在1 s内达到30 mV）; （iii）快速（5 s）重新极化。 [Ca2 +] i在（i）期间降低，在（ii）期间迅速增加，峰值消极延迟为1 s，在（iii）期间降低。 5.轻微的去极化会增加振荡频率，而大的去极化会降低振荡频率。 6.依赖Ca（2+）的K +通道阻滞剂apamin增加了持续时间，并降低了振荡频率。 7.我们提出了以下振荡机制：（i）膜电导率的降低可能是由于[Ca2 +] i的逐渐降低引起的钾电导（gK）的降低而使去极化缓慢。 （ii）达到激活Na +通道的阈值（由VTD降低），产生进一步的去极化和募集Ca2 +通道，并且Ca2 +和VTD中毒的Na +通道的失活都很缓慢; （iii）gK增加，由增加的[Ca2 +] i激活Ca（2+）依赖性K +通道，从而使膜重新极化。 Na +通道的贡献似乎对于产生振荡至关重要。 8.牛嗜铬细胞具有[Ca2 +] i振荡所需的机制，尽管此处测试的更多生理刺激（高K +，场电刺激，烟碱或毒蕈碱激动剂）主要产生了非振荡反应。

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