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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Ba2+ ions evoke two kinetically distinct patterns of exocytosis in chromaffin cells, but not in neurohypophysial nerve terminals.
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Ba2+ ions evoke two kinetically distinct patterns of exocytosis in chromaffin cells, but not in neurohypophysial nerve terminals.

机译：Ba2 +离子在嗜铬细胞中引起两种动力学上不同的胞吐作用，而在神经下垂体神经末梢则不起作用。

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摘要

The coupling between divalent cations and exocytosis of large dense-cored vesicles (LDCV) was studied with capacitance-detection techniques in nerve terminals of the rat neurohypophysis (NHP) and bovine chromaffin cells. Ba2+ substitution for Ca2+ produced kinetically distinct responses in the two preparations. In NHP terminals, Ba2+ ions behave as weak substitutes for Ca2+. Exocytotic events occur principally during depolarizing pulses, i.e., events are "stimulus-coupled" to Ba2+ entry through voltage-gated Ca2+ channels. Stimulus-coupled exocytosis apparently requires elevated submembrane cation concentrations that dissipate rapidly on hyperpolarization-induced Ca(2+)-channel closure. Intracellular dialysis of NHP terminals with Ba2+ does not evoke exocytosis, nor does it interfere with depolarization-evoked Ca2+ influx and exocytosis. In chromaffin cells, Ba2+ ions evoke a small quantity of stimulus-coupled secretion, but the dominant response is an additional pronounced poststimulus capacitance increase that outlasts channel closures by 20-50 sec. "Stimulus-decoupled" exocytosis is slow (approximately 25-40 fF/sec) compared with Ca(2+)-evoked stimulus-coupled exocytosis (approximately 1000 fF/sec). Decoupled secretion is not attributable to Ba2+ displacement of intracellular Ca2+ ions, because it is insensitive to 10 mM EGTA or thapsigargin. Slow exocytosis is initiated by inclusion of Ba2+ ions in the recording pipette and continues steadily for 5-12 min, producing a total increase of several thousand fF, which ultimately doubles or triples the original cell-surface area. We propose that two pathways of regulated exocytosis with distinct kinetics and divalent cation sensitivity exist in chromaffin cells. Only a single kinetic pattern is detected in NHP terminals, suggesting that mechanisms for secretion are not universally distributed in excitable cells.
机译：在大鼠神经垂体（NHP）和牛嗜铬细胞的神经末梢，采用电容检测技术研究了二价阳离子与大密度核囊泡（LDCV）的胞吐作用之间的耦合。在两种制剂中，Ba2 +替代Ca2 +产生了动力学上不同的响应。在NHP终端中，Ba2 +离子充当Ca2 +的弱替代物。细胞外事件主要发生在去极化脉冲期间，即事件通过电压门控的Ca2 +通道与Ba2 +进入“刺激耦合”。刺激耦合的胞吐作用显然需要升高的超膜诱导的Ca（2+）通道关闭迅速消散的亚膜阳离子浓度。用Ba2 +对NHP末端进行细胞内透析不会引起胞吐作用，也不会干扰去极化引起的Ca2 +流入和胞吐作用。在嗜铬细胞中，Ba 2+离子引起少量的刺激性耦合分泌，但主要的反应是刺激后电容的明显增加，使通道闭合持续20-50秒。与Ca（2+）引起的刺激耦合胞吐作用（约1000 fF / sec）相比，“刺激解耦”胞吐作用较慢（约25-40 fF / sec）。解耦的分泌不能归因于细胞内Ca2 +离子的Ba2 +置换，因为它对10 mM EGTA或毒胡萝卜素不敏感。缓慢的胞吐作用始于记录移液管中包含Ba2 +离子，并稳定持续5-12分钟，从而产生数千fF的总增加量，最终使原始细胞表面积增加一倍或三倍。我们建议在嗜铬细胞中存在两条具有不同动力学和二价阳离子敏感性的调节胞吐途径。在NHP末端仅检测到单一动力学模式，这表明分泌机制并未在兴奋性细胞中普遍分布。

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