The loss of 45Ca 2+ associated with prolactin release from the tilapia ( Oreochromis mossambicus) rostral pars distalis

Abstract

The relationship between tritium 3H-labeled prolactin (PRL) release and the loss of tissue-associated 45Ca 2+ was examined in the tilapia rostral pars distalis (RPD) using perifusion incubation under conditions which inhibit or stimulate PRL release. Depolarizing [K +] (56 m M) and hyposmotic medium (280 mOsmolal) increased both the release of [ 3H]PRL and the loss of 45Ca 2+. The responses to high [K +] were faster and shorter in duration than those produced by reduced osmotic pressure. The depletion of Ca 2+ from the incubation medium with 2 m M EGTA suppressed the [ 3H]PRL response evoked by high [K +] or reduced osmotic pressure. Exposing the tissues to Ca 2+-depleted medium in the absence of high [K +] or reduced osmotic pressure produced a sharp, but brief, increase in 45Ca 2+ loss. Cobalt (10 −3 M), a competitive inhibitor of calcium-mediated processes, inhibited the [ 3H]PRL response to hyposmotic medium and to high [K +]. Cobalt also diminished the increased loss of 45Ca 2+ evoked by exposure to reduced osmotic pressure, but was ineffective in altering responses to high [K +]. Methoxyverapamil (D600; 10 −5 M), a blocker of certain voltage-sensitive Ca 2+ channels, did not alter either the [ 3H]PRL or the 45Ca 2+ responses to high [K +] and reduced osmotic pressure. Taken together with our earlier studies, the present findings suggest that exposure to high [K +] or hyposmotic medium produces rapid changes in the Ca 2+ metabolism of the tilapia RPD that are linked to the stimulation of PRL secretion. Nevertheless, the increased 45Ca 2+ loss, but not [ 3H]PRL release, upon exposure to Ca 2+-depleted media suggests that Ca 2+ loss may not always reflect intracellular events that lead to PRL release.