In vitro and in vivo evidence that dopamine exerts growth hormone-releasing activity in goldfish

Abstract

We have previously demonstrated that dopamine (DA) and the DA D1 agonist SKF 38393 stimulate growth hormone (GH) release from perifused pituitary fragments of the goldfish, suggesting an involvement of DA D1 receptors in GH regulation. In the present study, the role of DA on GH release and body growth of the goldfish was further investigated both in vivo and in vitro. DA consistently stimulated GH release in a dose-dependent manner from perifused goldfish pituitary fragments. The GH-releasing action of DA was seasonal, being the highest in sexually regressed fish, intermediate in recrudescent fish, and the lowest in sexually mature (prespawning) fish. Somatostatin, a known GH-release inhibitor in the goldfish, suppressed basal GH release and abolished the GH response to DA in perifused pituitary fragments as well as pituitary cells under static incubation. Intraperitoneal administration of the nonselective DA agonist apomorphine and the D1 agonist SKF 82958 increased the plasma GH levels in the goldfish. These GH responses were blocked by simultaneous treatment with the D1 antagonist Sch 23390 but not the D2 antagonist pimozide. Apomorphine administered orally also induced a similar elevation in plasma GH levels. Long-term feeding with apomorphine was found to be stimulatory to the body growth of goldfish. These results provide evidence that the neurotransmitter DA, by acting through DA D1 receptors in the pituitary, also functions as a GH-releasing factor in the goldfish.