Differential Actions of Dopamine Receptor Subtypes on Gonadotropin and Growth Hormone Release in vitro in Goldfish

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Abstract
Incubation of cultured goldfish pituitary cells with 10 nM to 1 .mu.M apomorphine (APO), a non-selective dopamine agonist, increased growth hormone (GH) release in a dose-dependent manner. GH release was also stimulated in a dose-dependent manner by 0.1 mM to 1 .mu.M salmon gonadotropin (GTH)-releasing hormone (sGnRH), sGnRH analog, and chicken GnRH-II (cGnRH-II). The magnitude of GH responses to 1 .mu.M GnRHs were less that to 1 .mu.M APO. GH responses to 10 nM to 1 .mu.M APO were not significantly increased by the addition of GnRHs. Static incubations with 0.1 mM to 1 .mu.M of the dopamine D1 agonist SKF38393 did not alter basal GTH release, or the GTH responses to 10 nM sGnRH and cGnRH-II. In contrast, the D1 agonist SKF38393 significantly increased basal GH secretion with maximal stimulation achieved at 100 nM concentrations, and GH responses to 10 nM sGnRH and 10 nM cGnRH-II were enhanced by simultaneous applications of SKF38393. Incubation with 1 .mu.M of the D2 agonist LY171555 decreased basal GTH release. Additions of 0.1 nM to 1 .mu.M LY171555 caused dose-dependent decreases in the GTH secretion induced by 10 nM sGnRH and cGnRH-II. In contrast, basal and GnRH-stimulated GH release were not affected by coincubations with LY171555. The D1 antagonist SKF83566 and the D2 antagonist domperidone at 1 .mu.M concentrations, specifically blocked the D1 agonist SKF38393-stimulated increase in GH release and the D2 agonist LY171555-induced depression of GTH secretion, respectively. In cell column perifusion studies, the D1 agonist SKF38393 at 0.1 nM to 1 .mu.M had no effects on GTH release, but significantly elevated GH secretion rates when applied at 0.1-1 .mu.M concentrations. The GH release induced by 1 .mu.M SKF38393 was significantly reduced by simultaneous perifusion with 1 .mu.M of the D1 antagonist SKF83566. Treatments with SKF83566 did not affect net GTH and GH responses to sGnRH challenges. In contrast, perifusion with 0.1 and 1 .mu.M of the D2 agonist LY1714555 depressed basal as well as sGnRH-induced GTH responses. These effects of 1 .mu.M LY171555 were completely blocked by simultaneous applications of 1 .mu.M domperidone, a D2 antagonist. Treatments with these D2 selective drugs did not affect basal and sGnRH-stimulated GH release. These results indicate that in cultured goldfish pituitary cells, activation of dopamine D1- and D2-like receptors specifically stimulates GH release and inhibits both basal and stimulated GTH secretion, respectively. The presence of direct actions of sGnRH and cGnRH-II on goldfish GTH an GH release are also demonstrated. This is the first study do demonstrate stimulatory dopamine D1 actions in the vertebrate pituitary.

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