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Article: Norepinephrine regulation of growth hormone release from goldfish pituitary cells. II. Intracellular sites of action

TitleNorepinephrine regulation of growth hormone release from goldfish pituitary cells. II. Intracellular sites of action
Authors
Issue Date2000
PublisherBlackwell Publishing Ltd.
Citation
Journal Of Neuroendocrinology, 2000, v. 12 n. 4, p. 323-333 How to Cite?
AbstractPrevious results suggest that norepinephrine decreases growth hormone (GH) release in goldfish by means of α-2 adrenoceptor activation. The intracellular mechanisms by which norepinephrine inhibits GH release were examined in the present study using dispersed goldfish pituitary cells. In 2-h static incubation experiments, norepinephrine and the α-2 agonist clonidine decreased basal GH release and the GH responses to stimulation by the dopamine D1 agonist SKF38393 and two native gonadotropin-releasing hormones (GnRH). Norepinephrine also reduced GH responses to the adenylate cyclase activator forskolin, two protein kinase C (PKC) activators (phorbol ester and synthetic diacylglycerol), and two Ca2+ ionophores (ionomycin and A23187). Similarly, norepinephrine applied as a 1-h pulse in cell column perifusion experiments reduced basal GH release and abolished the GH response to a 5-min pulse of arachidonic acid. In goldfish, D1-stimulated GH release is mediated by AC-, arachidonic acid-and Ca2+-dependent pathways, whereas GnRH action is coupled to PKC-and Ca2+-dependent mechanisms. These results suggest that norepinephrine activation of α-2 receptors inhibits ligand-induced GH secretion by actions subsequent to activation of these second messenger cascades. To further characterize norepinephrine mechanisms of action on unstimulated hormone release, the ability of norepinephrine and an α-2 agonist to affect activation of two second messenger cascades under basal conditions was also investigated. Static incubation with clonidine reduced cAMP production in a time-and dose-dependent manner, suggesting that norepinephrine inhibitory action can also be expressed at the level of cAMP production. Resting intracellular free calcium levels in single, identified goldfish somatotropes was unaffected by norepinephrine. However, the inhibitory effects of norepinephrine on basal GH secretion was not observed in the presence of a voltage-sensitive Ca2+ channel agonist. Whether these channels are targets for norepinephrine action on unstimulated GH release requires further investigation.
Persistent Identifierhttp://hdl.handle.net/10722/84617
ISSN
2015 Impact Factor: 3.172
2015 SCImago Journal Rankings: 1.541
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYunker, WKen_HK
dc.contributor.authorLee, EKYen_HK
dc.contributor.authorWong, AOLen_HK
dc.contributor.authorChang, JPen_HK
dc.date.accessioned2010-09-06T08:55:08Z-
dc.date.available2010-09-06T08:55:08Z-
dc.date.issued2000en_HK
dc.identifier.citationJournal Of Neuroendocrinology, 2000, v. 12 n. 4, p. 323-333en_HK
dc.identifier.issn0953-8194en_HK
dc.identifier.urihttp://hdl.handle.net/10722/84617-
dc.description.abstractPrevious results suggest that norepinephrine decreases growth hormone (GH) release in goldfish by means of α-2 adrenoceptor activation. The intracellular mechanisms by which norepinephrine inhibits GH release were examined in the present study using dispersed goldfish pituitary cells. In 2-h static incubation experiments, norepinephrine and the α-2 agonist clonidine decreased basal GH release and the GH responses to stimulation by the dopamine D1 agonist SKF38393 and two native gonadotropin-releasing hormones (GnRH). Norepinephrine also reduced GH responses to the adenylate cyclase activator forskolin, two protein kinase C (PKC) activators (phorbol ester and synthetic diacylglycerol), and two Ca2+ ionophores (ionomycin and A23187). Similarly, norepinephrine applied as a 1-h pulse in cell column perifusion experiments reduced basal GH release and abolished the GH response to a 5-min pulse of arachidonic acid. In goldfish, D1-stimulated GH release is mediated by AC-, arachidonic acid-and Ca2+-dependent pathways, whereas GnRH action is coupled to PKC-and Ca2+-dependent mechanisms. These results suggest that norepinephrine activation of α-2 receptors inhibits ligand-induced GH secretion by actions subsequent to activation of these second messenger cascades. To further characterize norepinephrine mechanisms of action on unstimulated hormone release, the ability of norepinephrine and an α-2 agonist to affect activation of two second messenger cascades under basal conditions was also investigated. Static incubation with clonidine reduced cAMP production in a time-and dose-dependent manner, suggesting that norepinephrine inhibitory action can also be expressed at the level of cAMP production. Resting intracellular free calcium levels in single, identified goldfish somatotropes was unaffected by norepinephrine. However, the inhibitory effects of norepinephrine on basal GH secretion was not observed in the presence of a voltage-sensitive Ca2+ channel agonist. Whether these channels are targets for norepinephrine action on unstimulated GH release requires further investigation.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltd.en_HK
dc.relation.ispartofJournal of Neuroendocrinologyen_HK
dc.rightsJournal of Neuroendocrinology. Copyright © Blackwell Publishing Ltd.en_HK
dc.titleNorepinephrine regulation of growth hormone release from goldfish pituitary cells. II. Intracellular sites of actionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0953-8194&volume=12&spage=323&epage=333&date=2000&atitle=Norepinephrine+Regulation+of+Growth+Hormone+Release+from+Goldfish+Pituitary+Cells.+II.+Intracellular+Sites+of+Action.en_HK
dc.identifier.emailWong, AOL: olwong@hkucc.hku.hken_HK
dc.identifier.authorityWong, AOL=rp00806en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1046/j.1365-2826.2000.00456.xen_HK
dc.identifier.pmid10718929-
dc.identifier.scopuseid_2-s2.0-0034016992en_HK
dc.identifier.hkuros53245en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034016992&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume12en_HK
dc.identifier.issue4en_HK
dc.identifier.spage323en_HK
dc.identifier.epage333en_HK
dc.identifier.isiWOS:000086268600006-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridYunker, WK=24449778300en_HK
dc.identifier.scopusauthoridLee, EKY=7406968652en_HK
dc.identifier.scopusauthoridWong, AOL=7403147570en_HK
dc.identifier.scopusauthoridChang, JP=7601547649en_HK

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