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Article: Cyclic 3',5'-adenosine monophosphate mediates dopamine D1-stimulated growth hormone release from goldfish pituitary cells

TitleCyclic 3',5'-adenosine monophosphate mediates dopamine D1-stimulated growth hormone release from goldfish pituitary cells
Authors
Issue Date1994
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/NEN
Citation
Neuroendocrinology, 1994, v. 60 n. 4, p. 410-417 How to Cite?
AbstractPreviously, we have demonstrated that dopamine (DA) stimulates growth hormone (GH) release from the goldfish pituitary through DA D1 receptors. In the present study, the role of cAMP in DA D1-stimulated GH release was investigated using static incubation of goldfish pituitary cells. The D1 agonist SKF38393 (1 nM-10 microM) induced GH release and cAMP accumulation in a dose-dependent manner with ED50s of 73 +/- 32 and 109 +/- 53 nM, respectively. In contrast, the D2 agonist LY171555 (1 nM-10 microM) was not effective in these regards. The GH-releasing action of SKF38393 was mimicked by the adenylate cyclase activator forskolin (0.1-40 microM) as well as the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (0.1 microM-1 mM). Dideoxyforskolin (0.1-40 microM), a derivative of forskolin inactive in stimulating adenylate cyclase, did not affect basal GH secretion. Similar stimulatory effects on GH release were also observed using the membrane-permeant cAMP analogs (10 microM-2 mM), dibutyryl cAMP and 8-bromo cAMP (8Br.cAMP). In the presence of a high dose (1 mM) of Br.cAMP, the ability of SKF38393 (1 nM-10 microM) to stimulate GH release was abolished, suggesting that the GH-releasing actions of cAMP and DA D1 stimulation are mediated through a common signal transduction mechanism. In the present study, the possible involvement of the cAMP-dependent enzyme protein kinase A (PKA) in DA D1-stimulated GH release was also examined. The GH responses to 8Br.cAMP (1 mM) and SKF38393 (1 microM) were blocked by simultaneous treatment with the PKA inhibitor H89 (10 microM).(ABSTRACT TRUNCATED AT 250 WORDS)
Persistent Identifierhttp://hdl.handle.net/10722/84952
ISSN
2015 Impact Factor: 2.583
2015 SCImago Journal Rankings: 1.479

 

DC FieldValueLanguage
dc.contributor.authorWong, AOLen_HK
dc.contributor.authorVan Der Kraak, Gen_HK
dc.contributor.authorChang, JPen_HK
dc.date.accessioned2010-09-06T08:59:01Z-
dc.date.available2010-09-06T08:59:01Z-
dc.date.issued1994en_HK
dc.identifier.citationNeuroendocrinology, 1994, v. 60 n. 4, p. 410-417en_HK
dc.identifier.issn0028-3835en_HK
dc.identifier.urihttp://hdl.handle.net/10722/84952-
dc.description.abstractPreviously, we have demonstrated that dopamine (DA) stimulates growth hormone (GH) release from the goldfish pituitary through DA D1 receptors. In the present study, the role of cAMP in DA D1-stimulated GH release was investigated using static incubation of goldfish pituitary cells. The D1 agonist SKF38393 (1 nM-10 microM) induced GH release and cAMP accumulation in a dose-dependent manner with ED50s of 73 +/- 32 and 109 +/- 53 nM, respectively. In contrast, the D2 agonist LY171555 (1 nM-10 microM) was not effective in these regards. The GH-releasing action of SKF38393 was mimicked by the adenylate cyclase activator forskolin (0.1-40 microM) as well as the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (0.1 microM-1 mM). Dideoxyforskolin (0.1-40 microM), a derivative of forskolin inactive in stimulating adenylate cyclase, did not affect basal GH secretion. Similar stimulatory effects on GH release were also observed using the membrane-permeant cAMP analogs (10 microM-2 mM), dibutyryl cAMP and 8-bromo cAMP (8Br.cAMP). In the presence of a high dose (1 mM) of Br.cAMP, the ability of SKF38393 (1 nM-10 microM) to stimulate GH release was abolished, suggesting that the GH-releasing actions of cAMP and DA D1 stimulation are mediated through a common signal transduction mechanism. In the present study, the possible involvement of the cAMP-dependent enzyme protein kinase A (PKA) in DA D1-stimulated GH release was also examined. The GH responses to 8Br.cAMP (1 mM) and SKF38393 (1 microM) were blocked by simultaneous treatment with the PKA inhibitor H89 (10 microM).(ABSTRACT TRUNCATED AT 250 WORDS)-
dc.languageengen_HK
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/NENen_HK
dc.relation.ispartofNeuroendocrinologyen_HK
dc.rightsNeuroendocrinology. Copyright © S Karger AG.en_HK
dc.subject.meshCyclic AMP - analogs and derivatives - physiology-
dc.subject.meshDopamine Agonists - pharmacology-
dc.subject.meshGoldfish - metabolism-
dc.subject.meshGrowth Hormone - metabolism-
dc.subject.meshPituitary Gland - cytology - metabolism-
dc.titleCyclic 3',5'-adenosine monophosphate mediates dopamine 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.doi10.1159/000126775-
dc.identifier.pmid7529899-
dc.identifier.hkuros5758en_HK
dc.identifier.volume60-
dc.identifier.issue4-
dc.identifier.spage410-
dc.identifier.epage417-
dc.publisher.placeSwitzerland-

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