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Effects of Corticotrophin Releasing Factor, Muscarine and Somatostatin on Rubidium and Potassium Efflux from Mouse AtT‐20 Pituitary Cells
Author(s) -
Luini A.,
Brown D. A.
Publication year - 1990
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.1990.tb00404.x
Subject(s) - muscarine , chemistry , efflux , somatostatin , endocrinology , medicine , oxotremorine , forskolin , tetraethylammonium , acetylcholine , potassium channel , charybdotoxin , potassium , biochemistry , muscarinic acetylcholine receptor , biology , receptor , organic chemistry
Effects of secretagogues and anti‐secretagogues of ACTH secretion on K + permeability in the clonal pituitary cell line AtT‐20 were measured by recording 86 Rb or 42 K efflux. Efflux was accelerated by the secretagogues K + , corticotrophin, forskolin, isoprenaline, and the Ca‐ionophore A23187. Efflux was reduced by the inhibitors somatostatin, muscarine, and oxotremorine, or by removing external Ca. Efflux was also reduced by the K + ‐channel blocking compound d‐tubocurarine but not by tetraethylammonium. Muscarine, oxotremorine, somatostatin, and 0 Ca 2+ also reduced intracellular Ca 2+ measured by quin‐2 fluorescence. It is suggested that most of the resting 86 Rb or 42 K efflux measured under these conditions occurs via tubocurarine‐sensitive Ca 2+ ‐dependent K + ‐channels, and that changes in efflux rate produced by secretagogues or anti‐secretagogues are secondary to changes in intracellular Ca 2+ .