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Article: Role of arachidonic acid and calmodulin in mediating dopamine D1- and GnRH-stimulated growth hormone release in goldfish pituitary cells

TitleRole of arachidonic acid and calmodulin in mediating dopamine D1- and GnRH-stimulated growth hormone release in goldfish pituitary cells
Authors
Issue Date1996
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ygcen
Citation
General And Comparative Endocrinology, 1996, v. 102 n. 1, p. 88-101 How to Cite?
AbstractIn goldfish, growth hormone (GH) release is stimulated by dopamine via D1 receptors and cAMP-dependent mechanisms and by gonadotropin-releasing hormone (GnRH) through a protein kinase C (PKC) pathway; in addition, both D1 and GnRH actions require extracellular Ca2+. In this study, the involvement of arachidonic acid (AA) and calmodulin (CaM) in mediating the GH responses to D1 and GnRH stimulation was examined using primary cultures of dispersed goldfish pituitary cells. In 2-hr static incubation experiments, the phospholipase A2 inhibitor bromophenacylbromide (BPB; 50 μM) decreased the GH responses to the D1 agonist SKF38393 (1 μM), the adenylate cyclase activator forskolin (10 μM), and the cAMP analog 8Br-cAMP (1 mM), but not the responses to salmon (s)GnRH (100 nM), chicken (c)GnRH-II (100 nM), and AA (50 μM). Similarly, the phospholipase A2 inhibitor quinacrine (50 μM) and an inhibitor of AA metabolism, nordihydroguaiaretic acid (NDGA; 50 μM), reduced the GH responses to SKF38393, forskolin, and 8Br-cAMP. The response to the dopamine agonist apomorphine (1 μM) was also decreased by NDGA. The GH responses to AA did not add to those of forskolin or SKF38393, but were additive to responses to sGnRH and the PKC activator tetradecanoyl phorbol acetate (TPA; 100 nM). In perifusion experiments, treatment with BPB reduced the acute GH response to 1 μM SKF38393, 10 μM forskolin, or 1 mM 8Br-cAMP. Taken together, these results suggest that mobilization and metabolism of AA mediate both acute and prolonged GH responses to D1, but not GnRH. The involvement of AA probably occurs distal to D1-induced cAMP generation. Two- hour static incubation with 10 nM to 10 μM KN62, a CaM-dependent kinase II inhibitor, decreased the GH response to 100 nM sGnRH or cGnRH-II. KN62 (1 μM) similarly decreased the GH response to 1 μM SKF38393, 10 μM forskolin, 1 mM 8Br-cAMP, or 100 nM TPA. In perifusion studies, KN62 (1 μM) also reduced the acute GH response to 5-min pulses of 100 nM sGnRH, 100 nM cGnRH- II, or 1 μM SKF38393. These results indicate that CaM mediates the acute, as well as the prolonged, GH responses to GnRH and dopamine. The involvement of CaM likely occurs distal to cAMP and PKC.
Persistent Identifierhttp://hdl.handle.net/10722/178587
ISSN
2015 Impact Factor: 2.667
2015 SCImago Journal Rankings: 1.245
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChang, JPen_US
dc.contributor.authorAbele, JTen_US
dc.contributor.authorVan Goor, Fen_US
dc.contributor.authorWong, AOLen_US
dc.contributor.authorNeumann, CMen_US
dc.date.accessioned2012-12-19T09:48:31Z-
dc.date.available2012-12-19T09:48:31Z-
dc.date.issued1996en_US
dc.identifier.citationGeneral And Comparative Endocrinology, 1996, v. 102 n. 1, p. 88-101en_US
dc.identifier.issn0016-6480en_US
dc.identifier.urihttp://hdl.handle.net/10722/178587-
dc.description.abstractIn goldfish, growth hormone (GH) release is stimulated by dopamine via D1 receptors and cAMP-dependent mechanisms and by gonadotropin-releasing hormone (GnRH) through a protein kinase C (PKC) pathway; in addition, both D1 and GnRH actions require extracellular Ca2+. In this study, the involvement of arachidonic acid (AA) and calmodulin (CaM) in mediating the GH responses to D1 and GnRH stimulation was examined using primary cultures of dispersed goldfish pituitary cells. In 2-hr static incubation experiments, the phospholipase A2 inhibitor bromophenacylbromide (BPB; 50 μM) decreased the GH responses to the D1 agonist SKF38393 (1 μM), the adenylate cyclase activator forskolin (10 μM), and the cAMP analog 8Br-cAMP (1 mM), but not the responses to salmon (s)GnRH (100 nM), chicken (c)GnRH-II (100 nM), and AA (50 μM). Similarly, the phospholipase A2 inhibitor quinacrine (50 μM) and an inhibitor of AA metabolism, nordihydroguaiaretic acid (NDGA; 50 μM), reduced the GH responses to SKF38393, forskolin, and 8Br-cAMP. The response to the dopamine agonist apomorphine (1 μM) was also decreased by NDGA. The GH responses to AA did not add to those of forskolin or SKF38393, but were additive to responses to sGnRH and the PKC activator tetradecanoyl phorbol acetate (TPA; 100 nM). In perifusion experiments, treatment with BPB reduced the acute GH response to 1 μM SKF38393, 10 μM forskolin, or 1 mM 8Br-cAMP. Taken together, these results suggest that mobilization and metabolism of AA mediate both acute and prolonged GH responses to D1, but not GnRH. The involvement of AA probably occurs distal to D1-induced cAMP generation. Two- hour static incubation with 10 nM to 10 μM KN62, a CaM-dependent kinase II inhibitor, decreased the GH response to 100 nM sGnRH or cGnRH-II. KN62 (1 μM) similarly decreased the GH response to 1 μM SKF38393, 10 μM forskolin, 1 mM 8Br-cAMP, or 100 nM TPA. In perifusion studies, KN62 (1 μM) also reduced the acute GH response to 5-min pulses of 100 nM sGnRH, 100 nM cGnRH- II, or 1 μM SKF38393. These results indicate that CaM mediates the acute, as well as the prolonged, GH responses to GnRH and dopamine. The involvement of CaM likely occurs distal to cAMP and PKC.en_US
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ygcenen_US
dc.relation.ispartofGeneral and Comparative Endocrinologyen_US
dc.subject.meshAcetophenones - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshArachidonic Acid - Physiologyen_US
dc.subject.meshCalmodulin - Physiologyen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshDopamine - Pharmacologyen_US
dc.subject.meshDrug Interactionsen_US
dc.subject.meshEnzyme Inhibitors - Pharmacologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshGoldfish - Physiologyen_US
dc.subject.meshGonadotropin-Releasing Hormone - Pharmacologyen_US
dc.subject.meshGrowth Hormone - Secretionen_US
dc.subject.meshMaleen_US
dc.subject.meshPhospholipases A - Antagonists & Inhibitorsen_US
dc.subject.meshPhospholipases A2en_US
dc.subject.meshPituitary Gland - Cytology - Drug Effects - Secretionen_US
dc.subject.meshReceptors, Dopamine D1 - Agonistsen_US
dc.subject.meshStimulation, Chemicalen_US
dc.titleRole of arachidonic acid and calmodulin in mediating dopamine D1- and GnRH-stimulated growth hormone release in goldfish pituitary cellsen_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.doi10.1006/gcen.1996.0050en_US
dc.identifier.pmid8860313-
dc.identifier.scopuseid_2-s2.0-0030006126en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0030006126&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume102en_US
dc.identifier.issue1en_US
dc.identifier.spage88en_US
dc.identifier.epage101en_US
dc.identifier.isiWOS:A1996UJ87400012-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridChang, JP=7601547649en_US
dc.identifier.scopusauthoridAbele, JT=36901463500en_US
dc.identifier.scopusauthoridVan Goor, F=35845505200en_US
dc.identifier.scopusauthoridWong, AOL=7403147570en_US
dc.identifier.scopusauthoridNeumann, CM=16157956900en_US

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