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Abstract
Thyrotropin-releasing hormone stimulation of prolactin secretion from rat pituitary (GH3) cells is biphasic with a secretory burst (0-2 min) at a higher rate, followed by sustained secretion (beyond 2 min) at a lower rate. Based on the effects of calcium ionophores, K+ depolarization, and diacylglycerol (or phorbol esters), it was suggested that the secretory burst is dependent on elevation of cytoplasmic free calcium concentration [( Ca2+]i) whereas sustained secretion is mediated by lipid-activated protein phosphorylation. In this study, we pretreated GH3 cells with 0.03 mM arachidonic acid to abolish thyrotropin-releasing hormone-induced elevation of [Ca2+]i (Kolesnick, R. N., and Gershengorn, M. C. (1985) J. Biol. Chem. 260, 707-713). In control cells, basal secretion was 0.7 +/- 0.2 ng/10(6) cells/min which increased to 8.3 +/- 0.8 between 0 and 2 min after TRH and remained elevated at 3.3 +/- 0.2 between 2-10 min. In cells pretreated with arachidonic acid, TRH stimulated prolactin secretion to only 2.6 +/- 0.3 ng/10(6) cells/min between 0 and 2 min and to 3.2 +/- 0.2 between 2 to 10 min; these values are not different from each other nor from the response between 2 and 10 min in control cells. K+ depolarization, which elevates [Ca2+]i even in arachidonic acid-pretreated cells but does not affect lipid metabolism, caused only a secretory burst. Bovine serum albumin, which binds free arachidonic acid and reverses arachidonic acid inhibition of TRH-induced elevation of [Ca2+]i, reversed the inhibition of the secretory burst stimulated by TRH. These studies present direct evidence that the burst of prolactin secretion stimulated by TRH is dependent on an elevation of [Ca2+]i whereas the sustained phase of secretion is independent of such elevation.
Highlights
In cells pretreated with We report that arachidonic acid pretreatment of GH, cells arachidonic acid, TRH stimulated prolactin secretion abolished TRH stimulation of the burst phase of secretion to only2.6 f 0.3 ng/106cells/min between 0 and 2 min without affecting the sustained phase of secretion
During 0-2 min in cells exposed to arachidonic acid alone and no different ( p > 0.1) than rate stimulated by TRH in control cells
If the calcium elevation were directly responsible phore abolishes the burst phase of prolactin secretion for the rapid phase of secretion and releasable prolactin were (21).The findings that K+depolarization (28; for review, see stillpresent, elevation of [Ca2+Iito a level similar to that Ref. 34) (Table I) andstimulation by calcium ionophores (26, usually observed after TRH should still have caused a rapid 28) cause burst secretion of prolactin suggest that anelevation stimulation of prolaction secretion in arachidonic acid-pre- of [Ca2+Ipi er se may be sufficient to stimulate rapid secretion treated cells
Summary
Effect of arachidonic acid pretreatment on TRH stimulation of prolactin secretionfrom GH, cells, its reversal with BSA, and comparison withstimulation by K+ depolarization For experiments to determine the effect of arachidonic acid on TRH-induced prolactin secretion, cells were pretreated with arachidonic
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