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青蛙味觉细胞中对奎宁产生感受器电位的离子机制。

Ionic mechanism of generation of receptor potential in response to quinine in frog taste cell.

作者信息

Okada Y, Miyamoto T, Sato T

机构信息

Department of Physiology, Nagasaki University School of Dentistry, Japan.

出版信息

Brain Res. 1988 May 31;450(1-2):295-302. doi: 10.1016/0006-8993(88)91568-5.

DOI:10.1016/0006-8993(88)91568-5
PMID:3261192
Abstract

The ionic mechanism of generation of the receptor potential in a frog taste cell elicited by quinine-HCl (Q-HCl) was studied with an intracellular recording technique by replacing the superficial and interstitial fluids of the tongue with various saline solutions. The taste cells whose receptor membranes were adapted to normal saline and deionized water generated depolarizing receptor potentials at Q-HCl concentrations higher than 2 and 0.01 mM, respectively. The input resistance of taste cell during Q-HCl stimulation scarcely changed. The receptor potential did not change even when the membrane potential level was broadly changed. The magnitude of the receptor potential was increased by reducing the concentration of superficial Cl- on the taste receptor membrane, but was independent to the concentration of superficial Na+. Injection of Cl- into a taste cell increased the receptor potential to 170%. The magnitude of receptor potential was decreased to 20-30% by removing interstitial Na+ or Cl- or both surrounding the basolateral membrane of taste cell. Furosemide (1 mM) added to the interstitial fluid decreased the receptor potential to 15%, while interstitial ouabain (0.1 mM) and superficial SITS (0.1 mM) did not influence it. From these results, we conclude: (1) an electroneutral Na+/Cl- cotransport occurs through the basolateral membrane of a taste cell in the resting state, so that Cl- accumulates inside the cell. (2) Q-HCl stimulation induces the active secretion of Cl- across the taste receptor membrane, resulting in a depolarizing receptor potential.

摘要

采用细胞内记录技术,通过用各种盐溶液替换舌表面和间质液,研究了盐酸奎宁(Q-HCl)诱发的青蛙味觉细胞中感受器电位产生的离子机制。感受器膜适应于生理盐水和去离子水的味觉细胞,分别在Q-HCl浓度高于2 mM和0.01 mM时产生去极化感受器电位。Q-HCl刺激期间味觉细胞的输入电阻几乎不变。即使膜电位水平有很大变化,感受器电位也没有改变。降低味觉感受器膜表面Cl-的浓度可增加感受器电位的幅度,但与表面Na+的浓度无关。向味觉细胞内注入Cl-可使感受器电位增加到170%。去除味觉细胞基底外侧膜周围的间质Na+或Cl-或两者,感受器电位的幅度可降低到20%-30%。向间质液中加入呋塞米(1 mM)可使感受器电位降低到15%,而间质哇巴因(0.1 mM)和表面4-乙酰氨基-4'-异硫氰基芪-2,2'-二磺酸(SITS,0.1 mM)对其没有影响。根据这些结果,我们得出以下结论:(1)在静息状态下,味觉细胞的基底外侧膜发生电中性的Na+/Cl-协同转运,从而使Cl-在细胞内积累。(2)Q-HCl刺激诱导Cl-通过味觉感受器膜的主动分泌,导致去极化感受器电位。

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