蟾蜍肾上腺嗜铬细胞电反应的离子成分

Veronica Nassar-Gentina, Christian Bonansco, Mario Luxoro
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摘要

1. 采用超细电极(300 MOhm)原位研究了蟾蜍肾上腺染色质细胞膜的电学特性。在生理[K+] 0 (2 mM)存在时,静息膜电位(Vm)为−53±3.2 mV。Vm依赖于[K+] 0,由常场方程预测,PNaPK为0.163。一小部分(20%)被刺穿的细胞表现出自发的电活动,尽管在所有被检查的细胞中,注射去极化电流脉冲引起了重复的尖峰。我们测量的嗜铬细胞输入电阻(326±35 MOhm)比报道的牛分离嗜铬细胞的值要小得多,这表明蟾蜍肾上腺嗜铬细胞可能是电偶的。四乙基铵(TEA)增加了峰值的幅度和持续时间,可能抑制了向外的K+电流。在河豚毒素(TTX)存在的情况下,动作电位被取消,但如果添加TEA,它们会重新出现,这表明Na+和Ca2+电流都参与了尖峰的发生。正如预期的那样,乙酰胆碱(ACh)和尼古丁使细胞去极化,尽管它们并不总是引起电活动。麝香碱(10 ~ 100 μM)对乙酰胆碱和尼古丁诱导的Vm和去极化均无影响。由于毒蕈碱能抑制乙酰胆碱和尼古丁诱导的儿茶酚胺(catecholamine, CA)的分泌,因此我们认为毒蕈碱对蟾蜍体内CA释放的抑制可能发生在细胞膜以外的水平。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Ionic components of the electrical response of chromaffin cells from the toad (Caudiverbera caudiverbera) adrenal gland

1. Ultra fine tip muelectrodes (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 PNaPK 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 μM) 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.

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