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Article: Entry of extracellular calcium mediates dopamie D1-stimulated growth hormone release from goldfish pituitary cells

TitleEntry of extracellular calcium mediates dopamie D1-stimulated growth hormone release from goldfish pituitary cells
Authors
Issue Date1994
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ygcen
Citation
General and Comparative Endocrinology, 1994, v. 94 n. 3, p. 316-328 How to Cite?
AbstractUnlike mammals, the goldfish is unique in having dopamine (DA) D1 receptors in the anterior pituitary. In this species, DA stimulates growth hormone (GH) release via D1 receptors coupled to the cAMP-dependent pathway. To further examine the postreceptor mechanisms of this novel pituitary DA D1 system, the role of extracellular Ca2+ ([Ca2+]e] in mediating DA D1-stimulated GH release was studied using dispersed goldfish pituitary cells. The GH responses to DA (1 nM-10 microM), the D1 agonist SKF38393 (1 microM), and the Ca2+ ionophore A23187 (10 microM) were abolished by incubation with Ca(2+)-deficient medium. Incubation with depolarizing doses of KCl (10-25 mM), which activate voltage-sensitive Ca2+ channels (VSCC), induced GH release in a dose-dependent manner. In contrast, the VSCC blockers nifedipine (10 microM), nicardipine (10 microM), and verapamil (10 microM) and the inorganic competitor of Ca2+ entry CoCl2 (5 mM) blocked the GH responses to DA (1 microM) as well as SKF38393 (1 microM). These results strongly indicate that the entry of [Ca2+]e via VSCC is an essential part of the signal transduction mechanisms mediating DA D1-stimulated GH release in the goldfish. In this study, the possible interactions between the Ca(2+)- and cAMP-dependent pathways in DA-induced GH secretion were also investigated. The membrane-permeant cAMP analogue 8Br.cAMP (1 mM) and the adenylate cyclase activator forskolin (10 microM) stimulated GH release from goldfish pituitary cells. These GH responses were suppressed by incubation with Ca(2+)-deficient medium or with the VSCC blocker nifedipine (10 microM). Furthermore, the GH responses to forskolin (10 microM) and the nonselective DA agonist apomorphine (1 microM) were not additive to that of the Ca2+ ionophore A23187 (10 microM). These results suggest that [Ca2+]e entry induced by DA D1 stimulation occur at steps after activation of the cAMP-dependent pathway.
Persistent Identifierhttp://hdl.handle.net/10722/84865
ISSN
2015 Impact Factor: 2.667
2015 SCImago Journal Rankings: 1.245
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWong, AOLen_HK
dc.contributor.authorVan Goor, Fen_HK
dc.contributor.authorChang, JP-
dc.date.accessioned2010-09-06T08:58:01Z-
dc.date.available2010-09-06T08:58:01Z-
dc.date.issued1994en_HK
dc.identifier.citationGeneral and Comparative Endocrinology, 1994, v. 94 n. 3, p. 316-328en_HK
dc.identifier.issn0016-6480en_HK
dc.identifier.urihttp://hdl.handle.net/10722/84865-
dc.description.abstractUnlike mammals, the goldfish is unique in having dopamine (DA) D1 receptors in the anterior pituitary. In this species, DA stimulates growth hormone (GH) release via D1 receptors coupled to the cAMP-dependent pathway. To further examine the postreceptor mechanisms of this novel pituitary DA D1 system, the role of extracellular Ca2+ ([Ca2+]e] in mediating DA D1-stimulated GH release was studied using dispersed goldfish pituitary cells. The GH responses to DA (1 nM-10 microM), the D1 agonist SKF38393 (1 microM), and the Ca2+ ionophore A23187 (10 microM) were abolished by incubation with Ca(2+)-deficient medium. Incubation with depolarizing doses of KCl (10-25 mM), which activate voltage-sensitive Ca2+ channels (VSCC), induced GH release in a dose-dependent manner. In contrast, the VSCC blockers nifedipine (10 microM), nicardipine (10 microM), and verapamil (10 microM) and the inorganic competitor of Ca2+ entry CoCl2 (5 mM) blocked the GH responses to DA (1 microM) as well as SKF38393 (1 microM). These results strongly indicate that the entry of [Ca2+]e via VSCC is an essential part of the signal transduction mechanisms mediating DA D1-stimulated GH release in the goldfish. In this study, the possible interactions between the Ca(2+)- and cAMP-dependent pathways in DA-induced GH secretion were also investigated. The membrane-permeant cAMP analogue 8Br.cAMP (1 mM) and the adenylate cyclase activator forskolin (10 microM) stimulated GH release from goldfish pituitary cells. These GH responses were suppressed by incubation with Ca(2+)-deficient medium or with the VSCC blocker nifedipine (10 microM). Furthermore, the GH responses to forskolin (10 microM) and the nonselective DA agonist apomorphine (1 microM) were not additive to that of the Ca2+ ionophore A23187 (10 microM). These results suggest that [Ca2+]e entry induced by DA D1 stimulation occur at steps after activation of the cAMP-dependent pathway.-
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ygcenen_HK
dc.relation.ispartofGeneral and Comparative Endocrinologyen_HK
dc.subject.meshCalcium - metabolism - physiology-
dc.subject.meshGoldfish - metabolism-
dc.subject.meshGrowth Hormone - metabolism-
dc.subject.meshPituitary Gland, Anterior - cytology - drug effects - metabolism-
dc.subject.meshReceptors, Dopamine D1 - agonists - physiology-
dc.titleEntry of extracellular calcium mediates dopamie D1-stimulated growth hormone release from goldfish pituitary cellsen_HK
dc.typeArticleen_HK
dc.identifier.emailWong, AOL: olwong@hkucc.hku.hken_HK
dc.identifier.authorityWong, AOL=rp00806en_HK
dc.identifier.doi10.1006/gcen.1994.1088-
dc.identifier.pmid7926640-
dc.identifier.hkuros5761en_HK
dc.identifier.volume94-
dc.identifier.issue3-
dc.identifier.spage316-
dc.identifier.epage328-
dc.identifier.isiWOS:A1994NT53800004-
dc.publisher.placeUnited States-

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