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Article: Interactions of cyclic adenosine 3',5'-monophosphate, protein kinase-C, and calcium in dopamine- and gonadotropin-releasing hormone-stimulated growth hormone release in the goldfish

TitleInteractions of cyclic adenosine 3',5'-monophosphate, protein kinase-C, and calcium in dopamine- and gonadotropin-releasing hormone-stimulated growth hormone release in the goldfish
Authors
Issue Date1994
PublisherThe Endocrine Society. The Journal's web site is located at http://endo.endojournals.org
Citation
Endocrinology, 1994, v. 135 n. 4, p. 1593-1604 How to Cite?
AbstractIn the goldfish, GH release is under the stimulatory control of multiple neuroendocrine factors, including dopamine (DA) and GnRH. We have previously shown that DA-stimulated GH release in the goldfish is mediated via D1 receptors and is dependent on cAMP, whereas the GH response to GnRH involves protein kinase-C (PKC) and extracellular Ca2+ entry through voltage- sensitive Ca2+ channels (VSCC). In this study, the interactions of PKC, cAMP, and Ca2+ in the regulation of GH release responses to DA and GnRH were examined using dispersed goldfish pituitary cells. The GnRH-induced GH secretion was unaffected by a protein kinase-A (PKA) inhibitor, but was additive to the GH responses to 8-bromo-cAMP (8-Br-cAMP), the phosphodiesterase inhibitor isobutylmethylxanthine, or the D1 agonist SKF38393. Similarly, the GH responses to PKC activators were additive to those to 8-Br-cAMP, forskolin, SKF38393, or the general DA agonist apomorphine. In contrast, depletion of cellular PKC content inhibited the GH responses to GnRH and PKC activators, but not those to DA, SKF38393, 8-Br- cAMP, or forskolin. Furthermore, the GH response to 8-Br-cAMP or SKF38393 was unaffected by the selective PKC inhibitor H7. Taken together, these results suggest that GnRH and DA D1 mechanisms stimulate GH release in the goldfish independently via PKC- and cAMP-dependent intracellular signaling pathways, respectively. However, both the cAMP (D1) and PKC (GnRH) mechanisms also interacted with VSCC. The VSCC agonist Bay K8644 potentiated, whereas the VSCC blocker verapamil reduced, the GH responses to GnRH, PKC activators, SKF38393, and activators of the cAMP pathway. A hypothesis is proposed based on these findings. GnRH and DA initiate GH release independently by activation of PKC- and cAMP-dependent mechanisms. The secondary activation of VSCC by either PKC or cAMP/PKA further enhances the GH response.
Persistent Identifierhttp://hdl.handle.net/10722/49433
ISSN
2015 Impact Factor: 4.159
2015 SCImago Journal Rankings: 2.363
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWong, AOLen_HK
dc.contributor.authorVan Goor, Fen_HK
dc.contributor.authorJobin, RMen_HK
dc.contributor.authorNeumann, CMen_HK
dc.contributor.authorChang, JPen_HK
dc.date.accessioned2008-06-12T06:42:32Z-
dc.date.available2008-06-12T06:42:32Z-
dc.date.issued1994en_HK
dc.identifier.citationEndocrinology, 1994, v. 135 n. 4, p. 1593-1604en_HK
dc.identifier.issn0013-7227en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49433-
dc.description.abstractIn the goldfish, GH release is under the stimulatory control of multiple neuroendocrine factors, including dopamine (DA) and GnRH. We have previously shown that DA-stimulated GH release in the goldfish is mediated via D1 receptors and is dependent on cAMP, whereas the GH response to GnRH involves protein kinase-C (PKC) and extracellular Ca2+ entry through voltage- sensitive Ca2+ channels (VSCC). In this study, the interactions of PKC, cAMP, and Ca2+ in the regulation of GH release responses to DA and GnRH were examined using dispersed goldfish pituitary cells. The GnRH-induced GH secretion was unaffected by a protein kinase-A (PKA) inhibitor, but was additive to the GH responses to 8-bromo-cAMP (8-Br-cAMP), the phosphodiesterase inhibitor isobutylmethylxanthine, or the D1 agonist SKF38393. Similarly, the GH responses to PKC activators were additive to those to 8-Br-cAMP, forskolin, SKF38393, or the general DA agonist apomorphine. In contrast, depletion of cellular PKC content inhibited the GH responses to GnRH and PKC activators, but not those to DA, SKF38393, 8-Br- cAMP, or forskolin. Furthermore, the GH response to 8-Br-cAMP or SKF38393 was unaffected by the selective PKC inhibitor H7. Taken together, these results suggest that GnRH and DA D1 mechanisms stimulate GH release in the goldfish independently via PKC- and cAMP-dependent intracellular signaling pathways, respectively. However, both the cAMP (D1) and PKC (GnRH) mechanisms also interacted with VSCC. The VSCC agonist Bay K8644 potentiated, whereas the VSCC blocker verapamil reduced, the GH responses to GnRH, PKC activators, SKF38393, and activators of the cAMP pathway. A hypothesis is proposed based on these findings. GnRH and DA initiate GH release independently by activation of PKC- and cAMP-dependent mechanisms. The secondary activation of VSCC by either PKC or cAMP/PKA further enhances the GH response.en_HK
dc.format.extent418 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherThe Endocrine Society. The Journal's web site is located at http://endo.endojournals.orgen_HK
dc.relation.ispartofEndocrinologyen_HK
dc.rightsEndocrinology. Copyright © The Endocrine Society.en_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshCalcium - metabolismen_HK
dc.subject.meshCyclic AMP - metabolismen_HK
dc.subject.meshDopamine - pharmacologyen_HK
dc.subject.meshGoldfish - metabolismen_HK
dc.subject.meshGonadotropin-releasing hormone - pharmacologyen_HK
dc.titleInteractions of cyclic adenosine 3',5'-monophosphate, protein kinase-C, and calcium in dopamine- and gonadotropin-releasing hormone-stimulated growth hormone release in the goldfishen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0013-7227&volume=135&issue=4&spage=1593&epage=1604&date=1994&atitle=Interactions+of+cyclic+adenosine+3%27,5%27-monophosphate,+protein+kinase-C,+and+calcium+in+dopamine-+and+gonadotropin-releasing+hormone-stimulated+growth+hormone+release+in+the+goldfishen_HK
dc.identifier.emailWong, AOL: olwong@hkucc.hku.hken_HK
dc.identifier.authorityWong, AOL=rp00806en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1210/en.135.4.1593en_HK
dc.identifier.pmid7925122-
dc.identifier.scopuseid_2-s2.0-0028017805en_HK
dc.identifier.hkuros5747-
dc.identifier.volume135en_HK
dc.identifier.issue4en_HK
dc.identifier.spage1593en_HK
dc.identifier.epage1604en_HK
dc.identifier.isiWOS:A1994PK87700040-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWong, AOL=7403147570en_HK
dc.identifier.scopusauthoridVan Goor, F=35845505200en_HK
dc.identifier.scopusauthoridJobin, RM=6701719589en_HK
dc.identifier.scopusauthoridNeumann, CM=16157956900en_HK
dc.identifier.scopusauthoridChang, JP=7601547649en_HK

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