Arachidonic acid increases cytosolic calcium and stimulates hormone
release in rat lactotrophs.
Roudbaraki, M. M., P. Vacher, and R. Drouhault.
Laboratoire de Neurophysiologie, Unit[acute]e de Recherche Associ[acute]ee
au Centre National de la Recherche Scientifique 1200, Universit[acute]e de
Bordeaux 2, 33076 Bordeaux C[acute]edex, France
APStracts 2:0015E, 1995.
Arachidonic acid (AA) released from membrane phospholipids following
activation of surface receptors, causes cellular signalling actions
in neurones and endocrine cells, including stimulation of prolactin
(PRL) release from dissociated rat pituitary cells and clonal cells
of the GH3 pituitary tumour line. In the present study, we
investigated the effect of exogenous AA on PRL release from dispersed
pituitary cells and tried to elucidate the mechanism involved in this
process. The effects of AA on cytosolic calcium concentration
([Ca2+]i) was studied using dual-emission
microspectrofluorimetry in identified lactotrophs and on PRL release
in dispersed pituitary cell populations. AA had a dose-dependent
effect on [Ca2+]i. At a concentration of 1 [mu]M, the Ca2+
increase was biphasic : a mobilization of intracellular calcium from
intracellular stores was followed by stimulation of Ca2+ influx. For
lower concentrations (10 and 100 nM), only the stimulation of Ca2+
influx was observed. AA-induced Ca2+ influx and PRL release were not
due to the stimulation of a PMA-sensitive protein kinase C. In the
same way, AA-stimulated PRL release and intracellular Ca2+ increase
were independent of intracellular thapsigargin-sensitive Ca2+ pools.
Furthermore, blockade of calcium channels suppressed AA-induced PRL
release. We hypothesize that Ca2+ influx plays a major role in AA
-induced PRL release.
Received 25 July 1994; accepted in final form 30 January 1995.
APS Manuscript Number E287-4.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 25 February 1995.