Signal transduction pathways in GnRH- and dopamine D1-stimulated growth hormone secretion in the goldfish.

Abstract

In goldfish, growth hormone (GH) secretion is regulated by multiple neuroendocrine factors. Among these regulators, gonadotropin-releasing hormone (GnRH) and dopamine (DA) are effective stimulators of GH release. The stimulatory actions of GnRH and DA are mediated by GnRH and DA D1 receptors on somatotropes, respectively. In this article, results from recent in vitro pharmacological and electrophysiological studies examining the possible involvement of extracellular Ca2+, protein kinase C, voltage-sensitive Ca2+ channels (VSCC) and phospholipase A2 in mediating GnRH-induced GH release are presented. Results from experiments investigating the possible interactions of cyclic adenosine 3',5'-monophosphate (cAMP), and extracellular Ca2+ entry through VSCC in mediating the DA D1-elicited GH response are also reported. These data were discussed in conjunction with other information available in the literature on the signal transduction mechanisms mediating GH secretion in goldfish. Based on these findings, a model for the transduction pathways integrating the initiation and maintenance of the distinct GnRH-induced and DA D1-elicited GH responses was proposed. GnRH and DA stimulate GH release via separate PKC- and cAMP-dependent mechanisms, respectively. These signalling mechanisms appear to act on distinct GH pools. PKC and cAMP subsequently activate VSCC. Ca2+ entry through VSCC plays a role in the sustained GH release response by enhancing the PKC- and cAMP-induced GH release.