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Article: Differential actions of dopamine receptor subtypes on gonadotropin and growth hormone release in vitro in goldfish

TitleDifferential actions of dopamine receptor subtypes on gonadotropin and growth hormone release in vitro in goldfish
Authors
Issue Date1990
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/NEN
Citation
Neuroendocrinology, 1990, v. 51 n. 6, p. 664-674 How to Cite?
AbstractIncubation of cultured goldfish pituitary cells with 10 nM to 1 μM 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 nM to 1 μM salmon gonadotropin (GTH)-releasing hormone (sGnRH), sGnRH analog, and chicken GnRH-II (cGnRH-II). The magnitude of GH responses to 1 μM GnRHs were less than that to 1 μM APO. GH responses to 10 nM to 1 μM APO were not significantly increased by the addition of GnRHs. Static incubations with 0.1 nM to 1 μM 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 concentration, and GH responses to 10 nM sGnRH and 10 nM cGnRH-II were enhanced by simultaneous applications of SKF38393. Incubation with 1 μM of the D2 agonist LY171555 decreased basal GTH release. Additions of 0.1 nM to 1 μM LY171555 caused dose-dependent decreases in the GTH secretion induced by 10 nM sGnRH and cGnR-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 μM 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 μM had no effects on GTH release, but significantly elevated GH secretion rates when applied at 0.1-1 μM concentrations. The GH release induced by 1 μM SKF38393 was significantly reduced by simultaneous perifusion with 1 μM of the D1 antagonist SKF83566. Treatments with SKF38393 and/or SKF83566 did not affect net GTH and GH responses to sGnRH challenges. In contrast, perifusion with 0.1 and 1 μM of the D2 agonist LY171555 depressed basal as well as sGnRH-induced GTH responses. These effects of 1 μM LY171555 were completely blocked by simultaneous applications of 1 μM 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 and GH release are also demonstrated. This is the first study do demonstrate stimulatory dopamine D1 actions in the vertebrate pituitary.
Persistent Identifierhttp://hdl.handle.net/10722/178494
ISSN
2015 Impact Factor: 2.583
2015 SCImago Journal Rankings: 1.479
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChang, JPen_US
dc.contributor.authorYu, KLen_US
dc.contributor.authorWong, AOLen_US
dc.contributor.authorPeter, REen_US
dc.date.accessioned2012-12-19T09:48:01Z-
dc.date.available2012-12-19T09:48:01Z-
dc.date.issued1990en_US
dc.identifier.citationNeuroendocrinology, 1990, v. 51 n. 6, p. 664-674en_US
dc.identifier.issn0028-3835en_US
dc.identifier.urihttp://hdl.handle.net/10722/178494-
dc.description.abstractIncubation of cultured goldfish pituitary cells with 10 nM to 1 μM 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 nM to 1 μM salmon gonadotropin (GTH)-releasing hormone (sGnRH), sGnRH analog, and chicken GnRH-II (cGnRH-II). The magnitude of GH responses to 1 μM GnRHs were less than that to 1 μM APO. GH responses to 10 nM to 1 μM APO were not significantly increased by the addition of GnRHs. Static incubations with 0.1 nM to 1 μM 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 concentration, and GH responses to 10 nM sGnRH and 10 nM cGnRH-II were enhanced by simultaneous applications of SKF38393. Incubation with 1 μM of the D2 agonist LY171555 decreased basal GTH release. Additions of 0.1 nM to 1 μM LY171555 caused dose-dependent decreases in the GTH secretion induced by 10 nM sGnRH and cGnR-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 μM 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 μM had no effects on GTH release, but significantly elevated GH secretion rates when applied at 0.1-1 μM concentrations. The GH release induced by 1 μM SKF38393 was significantly reduced by simultaneous perifusion with 1 μM of the D1 antagonist SKF83566. Treatments with SKF38393 and/or SKF83566 did not affect net GTH and GH responses to sGnRH challenges. In contrast, perifusion with 0.1 and 1 μM of the D2 agonist LY171555 depressed basal as well as sGnRH-induced GTH responses. These effects of 1 μM LY171555 were completely blocked by simultaneous applications of 1 μM 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 and GH release are also demonstrated. This is the first study do demonstrate stimulatory dopamine D1 actions in the vertebrate pituitary.en_US
dc.languageengen_US
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/NENen_US
dc.relation.ispartofNeuroendocrinologyen_US
dc.subject.mesh2,3,4,5-Tetrahydro-7,8-Dihydroxy-1-Phenyl-1H-3-Benzazepine - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshApomorphine - Pharmacologyen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCyprinidae - Physiologyen_US
dc.subject.meshDomperidone - Pharmacologyen_US
dc.subject.meshDopamine Antagonistsen_US
dc.subject.meshErgolines - Pharmacologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshGoldfish - Physiologyen_US
dc.subject.meshGonadotropins, Pituitary - Secretionen_US
dc.subject.meshGrowth Hormone - Secretionen_US
dc.subject.meshMaleen_US
dc.subject.meshPerfusionen_US
dc.subject.meshPituitary Gland - Drug Effects - Secretionen_US
dc.subject.meshPituitary Hormone-Releasing Hormones - Pharmacologyen_US
dc.subject.meshQuinpiroleen_US
dc.subject.meshReceptors, Dopamine - Physiologyen_US
dc.subject.meshReceptors, Dopamine D1en_US
dc.subject.meshReceptors, Dopamine D2en_US
dc.titleDifferential actions of dopamine receptor subtypes on gonadotropin and growth hormone release in vitro in goldfishen_US
dc.typeArticleen_US
dc.identifier.emailWong, AOL: olwong@hkucc.hku.hken_US
dc.identifier.authorityWong, AOL=rp00806en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1159/000125408-
dc.identifier.pmid2141920-
dc.identifier.scopuseid_2-s2.0-0025348520en_US
dc.identifier.volume51en_US
dc.identifier.issue6en_US
dc.identifier.spage664en_US
dc.identifier.epage674en_US
dc.identifier.isiWOS:A1990DJ27600009-
dc.publisher.placeSwitzerlanden_US
dc.identifier.scopusauthoridChang, JP=7601547649en_US
dc.identifier.scopusauthoridYu, KL=7403385265en_US
dc.identifier.scopusauthoridWong, AOL=7403147570en_US
dc.identifier.scopusauthoridPeter, RE=7202909690en_US

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