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牛肾上腺嗜铬细胞中的一种G蛋白激活的钾电流:在外排作用中可能的调节作用。

A G protein-activated K+ current in bovine adrenal chromaffin cells: possible regulatory role in exocytosis.

作者信息

Cannon S D, Wilson S P, Walsh K B

机构信息

Department of Pharmacology, University of South Carolina School of Medicine, Columbia 29208.

出版信息

Mol Pharmacol. 1994 Jan;45(1):109-16.

PMID:8302269
Abstract

Guanine nucleotide binding proteins (G proteins) act as signal transducers between membrane receptors and ion channels. In the present study, the whole-cell arrangement of the patch clamp technique was used to examine the effect of G proteins on K+ channels in cultured bovine adrenal chromaffin cells. Internal dialysis of chromaffin cells with guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S) or external application of AIF-4, to stimulate G proteins, resulted in a voltage-dependent increase in the amplitude of the outward K+ currents. The half-maximal voltage required for activation of the currents was shifted by -16 mV in the presence of GTP gamma S. The augmentation in the K+ currents was accompanied by the appearance of a fast component of current activation measured at potentials positive to 0 mV. The GTP gamma S-sensitive current could not be detected when internal K+ was replaced with Cs+ and was reversibly inhibited by tetraethylammonium (IC50, 2 mM). In contrast, the scorpion venom charybdotoxin (50 nM) and the bee venom apamin (250 nM) only slightly reduced the K+ currents during stimulation by GTP gamma S and did not alter the activation kinetics. In addition, the GTP gamma S-sensitive K+ current could be activated in the absence of internal Ca2+ and when the inward Ca2+ current was inhibited with CdCl2. Treatment of the chromaffin cells with fluoride decreased nicotine-evoked secretion of catecholamines in a concentration-dependent manner. Thus, bovine chromaffin cells contain a G protein-stimulated K+ channel that may play a regulatory role in secretagogue-mediated exocytosis.

摘要

鸟嘌呤核苷酸结合蛋白(G蛋白)作为膜受体与离子通道之间的信号转导分子。在本研究中,采用膜片钳技术的全细胞记录模式,检测G蛋白对培养的牛肾上腺嗜铬细胞钾通道的影响。用鸟苷5'-O-(3-硫代三磷酸)(GTPγS)对嗜铬细胞进行胞内透析,或外加AlF-4以激活G蛋白,均可使外向钾电流幅度呈电压依赖性增加。在存在GTPγS的情况下,激活电流所需的半数最大电压向负向移动了16 mV。钾电流的增大伴随着在高于0 mV电位时测得的电流激活快速成分的出现。当胞内钾被铯取代时,无法检测到对GTPγS敏感的电流,且该电流可被四乙铵可逆性抑制(半数抑制浓度,2 mM)。相反,蝎毒氯通道毒素(50 nM)和蜂毒阿帕明(250 nM)在GTPγS刺激过程中仅轻微降低钾电流,且不改变激活动力学。此外,在无胞内钙离子时以及用氯化镉抑制内向钙电流时,对GTPγS敏感的钾电流仍可被激活。用氟化物处理嗜铬细胞可浓度依赖性地降低尼古丁诱发的儿茶酚胺分泌。因此,牛嗜铬细胞含有一种受G蛋白刺激的钾通道,该通道可能在促分泌剂介导的胞吐作用中发挥调节作用。

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