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Article: Dopamine stimulates growth hormone release from the pituitary of goldfish, Carassius auratus, through the dopamine D1 receptors

TitleDopamine stimulates growth hormone release from the pituitary of goldfish, Carassius auratus, through the dopamine D1 receptors
Authors
Issue Date1992
PublisherThe Endocrine Society. The Journal's web site is located at http://endo.endojournals.org
Citation
Endocrinology, 1992, v. 130 n. 3, p. 1201-1210 How to Cite?
AbstractPreviously, we have demonstrated that ip injection of apomorphine, a nonselective dopamine (DA) agonist, increases serum GH levels in the goldfish, suggesting a possible role of DA in GH regulation. In the present study, the effects of DA on GH release in the goldfish were further characterized using an in vitro perifusion system for pituitary fragments. DA increased GH release in a dose-dependent manner with an ED50 of 0.26 ± 0.06 μM. SKF38393, a DA D1 agonist, mimicked the GH-releasing effect of DA with an ED50 of 0.41 ± 0.12 μM. Stereoselectivity consistent with mammalian DA D1 systems was demonstrated for the GH response to SKF38393; only the (+)- but not (-)-enantiomer of SKF38393 induced a dose-dependent GH release. Two other D1 agonists, SKF77434 and SKF82958, were also found to have GH-releasing activity. In contrast, high doses (up to 1 μM) of the DA D2 agonists, bromocriptine and LY171555, did not affect basal GH levels. The receptor specificity for DA-stimulated GH release was further investigated by using D1 and D2 antagonists; the D1 antagonists SCH23390 and SKF83566 completely abolished the GH response to DA or the D1 agonist SKF38393, whereas the D2-specific antagonists domperidone and (-)-sulpiride were not effective in this respect. Taken together, the present study demonstrates that DA is stimulatory to GH release from the pituitary of goldfish, and its action is mediated through receptors resembling the mammalian DA D1 receptors. The apparent similarities of the DA D1 receptor pharmacology between the goldfish and the mammals also indicate that D1 receptor is highly conserved during vertebrate evolution.
Persistent Identifierhttp://hdl.handle.net/10722/178527
ISSN
2021 Impact Factor: 5.051
2020 SCImago Journal Rankings: 1.674
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWong, AOLen_US
dc.contributor.authorChang, JPen_US
dc.contributor.authorPeter, REen_US
dc.date.accessioned2012-12-19T09:48:13Z-
dc.date.available2012-12-19T09:48:13Z-
dc.date.issued1992en_US
dc.identifier.citationEndocrinology, 1992, v. 130 n. 3, p. 1201-1210en_US
dc.identifier.issn0013-7227en_US
dc.identifier.urihttp://hdl.handle.net/10722/178527-
dc.description.abstractPreviously, we have demonstrated that ip injection of apomorphine, a nonselective dopamine (DA) agonist, increases serum GH levels in the goldfish, suggesting a possible role of DA in GH regulation. In the present study, the effects of DA on GH release in the goldfish were further characterized using an in vitro perifusion system for pituitary fragments. DA increased GH release in a dose-dependent manner with an ED50 of 0.26 ± 0.06 μM. SKF38393, a DA D1 agonist, mimicked the GH-releasing effect of DA with an ED50 of 0.41 ± 0.12 μM. Stereoselectivity consistent with mammalian DA D1 systems was demonstrated for the GH response to SKF38393; only the (+)- but not (-)-enantiomer of SKF38393 induced a dose-dependent GH release. Two other D1 agonists, SKF77434 and SKF82958, were also found to have GH-releasing activity. In contrast, high doses (up to 1 μM) of the DA D2 agonists, bromocriptine and LY171555, did not affect basal GH levels. The receptor specificity for DA-stimulated GH release was further investigated by using D1 and D2 antagonists; the D1 antagonists SCH23390 and SKF83566 completely abolished the GH response to DA or the D1 agonist SKF38393, whereas the D2-specific antagonists domperidone and (-)-sulpiride were not effective in this respect. Taken together, the present study demonstrates that DA is stimulatory to GH release from the pituitary of goldfish, and its action is mediated through receptors resembling the mammalian DA D1 receptors. The apparent similarities of the DA D1 receptor pharmacology between the goldfish and the mammals also indicate that D1 receptor is highly conserved during vertebrate evolution.en_US
dc.languageengen_US
dc.publisherThe Endocrine Society. The Journal's web site is located at http://endo.endojournals.orgen_US
dc.relation.ispartofEndocrinologyen_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.meshBenzazepines - Pharmacologyen_US
dc.subject.meshBromocriptine - Pharmacologyen_US
dc.subject.meshDomperidone - Pharmacologyen_US
dc.subject.meshDopamine - Pharmacologyen_US
dc.subject.meshDopamine Agents - Pharmacologyen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshErgolines - Pharmacologyen_US
dc.subject.meshGoldfish - Metabolism - Physiologyen_US
dc.subject.meshGonadotropin-Releasing Hormone - Antagonists & Inhibitors - Drug Effects - Metabolismen_US
dc.subject.meshGrowth Hormone - Blooden_US
dc.subject.meshPituitary Gland - Drug Effects - Metabolism - Ultrastructureen_US
dc.subject.meshQuinpiroleen_US
dc.subject.meshRadioimmunoassayen_US
dc.subject.meshReceptors, Dopamine - Drug Effects - Physiologyen_US
dc.titleDopamine stimulates growth hormone release from the pituitary of goldfish, Carassius auratus, through the dopamine D1 receptorsen_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.doi10.1210/en.130.3.1201en_US
dc.identifier.pmid1347006-
dc.identifier.scopuseid_2-s2.0-0026585854en_US
dc.identifier.volume130en_US
dc.identifier.issue3en_US
dc.identifier.spage1201en_US
dc.identifier.epage1210en_US
dc.identifier.isiWOS:A1992HG16100017-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridWong, AOL=7403147570en_US
dc.identifier.scopusauthoridChang, JP=7601547649en_US
dc.identifier.scopusauthoridPeter, RE=7202909690en_US
dc.identifier.issnl0013-7227-

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