大鼠垂体GH3细胞中的CCKB受体信号传导。CCK-8S通过Ca2+释放和Ca2+内流诱导细胞内钙动员。

CCKB receptor signaling in rat pituitary GH3 cells. CCK-8S-induced intracellular calcium mobilization by Ca2+ release and Ca2+ influx.

作者信息

Kaufmann R, Lindschau C, Schöneberg T, Henklein P, Boomgaarden M, Haller H, Ott T

机构信息

Institute of Pharmacology and Toxicology, Medical Faculty (Charité), Humboldt University of Berlin, Germany.

出版信息

Neuropeptides. 1994 Oct;27(4):211-6. doi: 10.1016/0143-4179(94)90001-9.

DOI:10.1016/0143-4179(94)90001-9

PMID:7808593

Abstract

We describe the effect of sulphated cholecystokinin octapeptide (CCK-8S) on [Ca2+]i in rat pituitary GH3 cells. Investigations were performed on fluo-3 loaded cells by using a confocal imaging system MRC-600 (Bio-Rad). Because CCK-8S mobilized intracellular calcium in cells bathed in Ca(2+)-free buffer it must be able to release calcium from internal stores. Furthermore, influx of Ca2+ from outside the cells seems to contribute to CCK-8S induced increases in [Ca2+]i as demonstrated by calcium mobilization in GH3 cells preincubated with thapsigargin in Ca2+ containing buffer.

摘要

我们描述了硫酸化胆囊收缩素八肽（CCK-8S）对大鼠垂体GH3细胞内钙离子浓度（[Ca2+]i）的影响。使用共聚焦成像系统MRC-600（伯乐公司）对加载了Fluo-3的细胞进行研究。由于CCK-8S能在无钙缓冲液中孵育的细胞中动员细胞内钙，所以它必定能够从细胞内储存库释放钙。此外，如在含Ca2+缓冲液中用毒胡萝卜素预孵育的GH3细胞中的钙动员所示，细胞外Ca2+的内流似乎也促成了CCK-8S诱导的[Ca2+]i升高。