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Dopamine‐D 2 Actions on Voltage‐Dependent Calcium Current and Gonadotropin‐II Secretion in Cultured Goldfish Gonadotrophs
Author(s) -
Van Goor Fredrick,
Goldberg Jeffrey I,
Chang John P
Publication year - 1998
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1046/j.1365-2826.1998.00812.x
Subject(s) - quinpirole , endocrinology , medicine , dopamine , agonist , chemistry , spiperone , dopamine receptor d2 , dopamine agonist , dopamine receptor , biology , receptor , dopaminergic
Dopamine D 2 ‐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 D 2 agonist, quinpirole, reduced GTH‐II secretion induced by either high extracellular K + concentration or the voltage‐gated Ca 2+ channel agonist, Bay K 8644. These actions of dopamine were blocked by addition of the dopamine D 2 ‐receptor antagonist, spiperone. The actions of dopamine on Ca 2+ current in single identified goldfish gonadotrophs were assessed in voltage‐clamp experiments using Ba 2+ as the charge carrier through voltage‐gated Ca 2+ channels. Dopamine caused a concentration‐dependent reduction in Ba 2+ current amplitude with an EC 50 of 1.0±0.3 nM, but did not shift the current‐voltage relationship. The D 2 agonist quinpirole also caused a dose‐dependent reduction in the Ba 2+ current amplitude with an EC 50 of 2.7±1.4 nM. Quinpirole slowed the activation and inactivation kinetics, as well as removing the steady‐state inactivation properties of the Ba 2+ current. In contrast to the actions of quinpirole, the dopamine D 1 ‐receptor agonist, SKF 38393, did not affect the Ba 2+ current. The inhibitory action of dopamine on voltage‐dependent Ca 2+ currents was reversed by spiperone, but not by the D 1 antagonist SKF 83566. Voltage‐dependent Na + and K + currents were not affected by dopamine or dopamine agonists. These data indicate that dopamine D 2 ‐receptor activation reduces Ca 2+ influx through voltage‐dependent Ca 2+ channels to inhibit GTH‐II secretion.