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蟾蜍(Caudiverbera caudiverbera)肾上腺嗜铬细胞电反应的离子成分。

Ionic components of the electrical response of chromaffin cells from the toad (Caudiverbera caudiverbera) adrenal gland.

作者信息

Nassar-Gentina V, Bonansco C, Luxoro M

机构信息

Laboratorio de Fisiologia Celular, Facultad de Ciencias, Universidad de Chile, Viña del Mar.

出版信息

Comp Biochem Physiol C Comp Pharmacol Toxicol. 1993 Jul;105(3):513-20. doi: 10.1016/0742-8413(93)90094-2.

DOI:10.1016/0742-8413(93)90094-2
PMID:7900970
Abstract
  1. Ultra fine tip microelectrodes (300 MOhm) were used to study the electrical properties of the chromaffin cell membrane in situ in the intact toad adrenal gland. 2. In the presence of physiologic [K+]o (2 mM) the resting membrane potential (Vm) was -53 +/- 3.2 mV. Vm depended on [K+]o as predicted by the constant field equation with PNa/PK of 0.16. 3. A small fraction (20%) of the impaled cells exhibited spontaneous electrical activity, though in all the cells examined, the injection of depolarizing current pulses elicited repetitive spikes. 4. Our measurements of the chromaffin cell input resistance (326 +/- 35 MOhm) is substantially smaller than the values reported for bovine isolated chromaffin cells, suggesting that the toad adrenal chromaffin cells might be electrically coupled. 5. Tetraethylammonium (TEA) increased the amplitude and duration of spikes, probably inhibiting outward K+ current. In the presence of tetrodotoxin (TTX) action potentials were abolished, although they reappeared if TEA was added, suggesting the participation of both Na+ and Ca2+ currents in the genesis of spikes. 6. As expected, acetylcholine (ACh) and nicotine depolarized the cells, though they did not always elicit electrical activity. 7. Muscarine (10-100 microM) had no effect on both Vm and on the depolarization induced by ACh or nicotine. Since muscarine inhibits catecholamine (CA) secretion induced by ACh and nicotine, we concluded that the inhibition of CA release by muscarine in the toad probably occurs at a level other than the membrane.
摘要
  1. 使用超微尖端微电极(300兆欧)研究完整蟾蜍肾上腺中嗜铬细胞膜的电特性。2. 在生理[K⁺]ₒ(2毫摩尔)存在的情况下,静息膜电位(Vm)为-53±3.2毫伏。Vm如恒定场方程所预测的那样取决于[K⁺]ₒ,PNa/PK为0.16。3. 一小部分(20%)被刺穿的细胞表现出自发电活动,不过在所有检测的细胞中,注入去极化电流脉冲会引发重复的尖峰。4. 我们测量的嗜铬细胞输入电阻(326±35兆欧)明显小于报道的牛分离嗜铬细胞的值,这表明蟾蜍肾上腺嗜铬细胞可能存在电耦合。5. 四乙铵(TEA)增加了尖峰的幅度和持续时间,可能是抑制了外向K⁺电流。在河豚毒素(TTX)存在的情况下,动作电位被消除,不过如果加入TEA,动作电位会再次出现,这表明Na⁺和Ca²⁺电流都参与了尖峰的产生。6. 正如预期的那样,乙酰胆碱(ACh)和尼古丁使细胞去极化,不过它们并不总是引发电活动。7. 毒蕈碱(10 - 100微摩尔)对Vm以及ACh或尼古丁诱导的去极化均无影响。由于毒蕈碱抑制ACh和尼古丁诱导的儿茶酚胺(CA)分泌,我们得出结论,蟾蜍中毒蕈碱对CA释放的抑制可能发生在膜以外的水平。

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