AJP - Endocrinology and Metabolism, Vol 268, Issue 6 E1215-E1223, Copyright © 1995 by American Physiological Society

ARTICLES

Arachidonic acid increases cytosolic calcium and stimulates hormone release in rat lactotrophs

M. M. Roudbaraki, P. Vacher and R. Drouhault
Laboratoire de Neurophysiologie, Unite de Recherche Associee au Centre National de la Recherche Scientifique 1200, Universite de Bordeaux 2, France.

Arachidonic acid (AA) released from membrane phospholipids after activation of surface receptors causes cellular signaling actions in neurons and endocrine cells, including stimulation of prolactin (PRL) release from dissociated rat pituitary cells and clonal cells of the GH3 pituitary tumor 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 Ca2+ concentration ([Ca2+]i) were studied using dual-emission microspectrofluorometry in identification lactotrophs and on PRL release in dispersed pituitary cell populations. AA had a dose-dependent effect on [Ca2+]i. At 1 microM, the Ca2+ increase was biphasic: a mobilization of intracellular Ca2+ 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 phorbol 12-myristate 13-acetate-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 Ca2+ channels suppressed AA-induced PRL release. We hypothesize that Ca2+ influx plays a major role in AA-induced PRL release.

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