title: Dopamine-D2 actions on voltage-dependent calcium current and gonadotropin-II secretion in cultured goldfish gonadotrophs.
abstract: Dopamine D2-receptor activation directly inhibits GnRH-induced gonadotropin-II (maturational gonadotropin, GTH-II) secretion from goldfish pituitary cells. In this study, we show that dopamine and its D2 agonist, quinpirole, reduced GTH-II secretion induced by either high extracellular K+ concentration or the voltage-gated Ca2+ channel agonist, Bay K 8644. These actions of dopamine were blocked by addition of the dopamine D2-receptor antagonist, spiperone. The actions of dopamine on Ca2+ current in single identified goldfish gonadotrophs were assessed in voltage-clamp experiments using Ba2+ as the charge carrier through voltage-gated Ca2+ channels. Dopamine caused a concentration-dependent reduction in Ba2+ current amplitude with an EC50 of 1.0+/-0.3 nM, but did not shift the current-voltage relationship. The D2 agonist quinpirole also caused a dose-dependent reduction in the Ba2+ current amplitude with an EC50 of 2.7+/-1.4 nM. Quinpirole slowed the activation and inactivation kinetics, as well as removing the steady-state inactivation properties of the Ba2+ current. In contrast to the actions of quinpirole, the dopamine D1-receptor agonist, SKF 38393, did not affect the Ba2+ current. The inhibitory action of dopamine on voltage-dependent Ca2+ currents was reversed by spiperone, but not by the D1 antagonist SKF 83566. Voltage-dependent Na+ and K+ currents were not affected by dopamine or dopamine agonists. These data indicate that dopamine D2-receptor activation reduces Ca2+ influx through voltage-dependent Ca2+ channels to inhibit GTH-II secretion.
authors.affiliation: Department of Biological Sciences, University of Alberta, Edmonton, Canada.
authors.forename: F
authors.initials: F
authors.lastname: Van Goor
authors.forename: J I
authors.initials: JI
authors.lastname: Goldberg
authors.forename: J P
authors.initials: JP
authors.lastname: Chang
mesh_terms: D000818:Animals; D001464:Barium / Q000502:physiology; D015220:Calcium Channels / Q000502:physiology*; D002478:Cells, Cultured; D004298:Dopamine / Q000494:pharmacology; D018491:Dopamine Agonists / Q000494:pharmacology; D004594:Electrophysiology; D006054:Goldfish / Q000502:physiology*; D006062:Gonadotropins / Q000378:metabolism*; D010902:Pituitary Gland / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D019257:Quinpirole / Q000494:pharmacology; D017447:Receptors, Dopamine D1 / Q000819:agonists; D017448:Receptors, Dopamine D2 / Q000819:agonists / Q000502:physiology*
chemical_list: D015220:Calcium Channels; D018491:Dopamine Agonists; D006062:Gonadotropins; D017447:Receptors, Dopamine D1; D017448:Receptors, Dopamine D2; D019257:Quinpirole; D001464:Barium; D004298:Dopamine