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Article: Mechanisms for gonadotropin-releasing hormone potentiation of growth hormone rebound following norepinephrine inhibition in goldfish pituitary cells

TitleMechanisms for gonadotropin-releasing hormone potentiation of growth hormone rebound following norepinephrine inhibition in goldfish pituitary cells
Authors
Issue Date2007
PublisherAmerican Physiological Society. The Journal's web site is located at http://ajpendo.physiology.org/
Citation
American Journal Of Physiology - Endocrinology And Metabolism, 2007, v. 292 n. 1, p. E203-E214 How to Cite?
AbstractIn the goldfish, norepinephrine (NE) inhibits growth hormone (GH) secretion through activation of pituitary α2-adrenergic receptors. Interestingly, a GH rebound is observed after NE withdrawal, which can be markedly enhanced by prior exposure to gonadotropin-releasing hormone (GnRH). Here we examined the mechanisms responsible for GnRH potentiation of this "postinhibition" GH rebound. In goldfish pituitary cells, α2-adrenergic stimulation suppressed both basal and GnRH-induced GH mRNA expression, suggesting that a rise in GH synthesis induced by GnRH did not contribute to its potentiating effect. Using a column perifusion approach, GnRH given during NE treatment consistently enhanced the GH rebound following NE withdrawal. This potentiating effect was mimicked by activation of PKC and adenylate cyclase (AC) but not by induction of Ca2+ entry through voltage-sensitive Ca2+ channels (VSCC). Furthermore, GnRH-potentiated GH rebound could be alleviated by inactivation of PKC, removal of extracellular Ca2+, blockade of VSCC, and inhibition of Ca 2+/calmodulin (CaM)-dependent protein kinase II (CaMKII). Inactivation of AC and PKA, however, was not effective in this regard. These results, as a whole, suggest that GnRH potentiation of GH rebound following NE inhibition is mediated by PKC coupled to Ca2+ entry through VSCC and subsequent activation of CaMKII. Apparently, the Ca2+-dependent cascades are involved in GH secretion during the rebound phase but are not essential for the initiation of GnRH potentiation. Since GnRH has been previously shown to have no effects on cAMP synthesis in goldfish pituitary cells, the involvement of cAMP-dependent mechanisms in GnRH potentiation is rather unlikely. Copyright © 2007 the American Physiological Society.
Persistent Identifierhttp://hdl.handle.net/10722/84681
ISSN
2015 Impact Factor: 3.825
2015 SCImago Journal Rankings: 2.465
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWong, AOLen_HK
dc.contributor.authorChuk, MCYen_HK
dc.contributor.authorHiu, CCen_HK
dc.contributor.authorLee, EKYen_HK
dc.date.accessioned2010-09-06T08:55:53Z-
dc.date.available2010-09-06T08:55:53Z-
dc.date.issued2007en_HK
dc.identifier.citationAmerican Journal Of Physiology - Endocrinology And Metabolism, 2007, v. 292 n. 1, p. E203-E214en_HK
dc.identifier.issn0193-1849en_HK
dc.identifier.urihttp://hdl.handle.net/10722/84681-
dc.description.abstractIn the goldfish, norepinephrine (NE) inhibits growth hormone (GH) secretion through activation of pituitary α2-adrenergic receptors. Interestingly, a GH rebound is observed after NE withdrawal, which can be markedly enhanced by prior exposure to gonadotropin-releasing hormone (GnRH). Here we examined the mechanisms responsible for GnRH potentiation of this "postinhibition" GH rebound. In goldfish pituitary cells, α2-adrenergic stimulation suppressed both basal and GnRH-induced GH mRNA expression, suggesting that a rise in GH synthesis induced by GnRH did not contribute to its potentiating effect. Using a column perifusion approach, GnRH given during NE treatment consistently enhanced the GH rebound following NE withdrawal. This potentiating effect was mimicked by activation of PKC and adenylate cyclase (AC) but not by induction of Ca2+ entry through voltage-sensitive Ca2+ channels (VSCC). Furthermore, GnRH-potentiated GH rebound could be alleviated by inactivation of PKC, removal of extracellular Ca2+, blockade of VSCC, and inhibition of Ca 2+/calmodulin (CaM)-dependent protein kinase II (CaMKII). Inactivation of AC and PKA, however, was not effective in this regard. These results, as a whole, suggest that GnRH potentiation of GH rebound following NE inhibition is mediated by PKC coupled to Ca2+ entry through VSCC and subsequent activation of CaMKII. Apparently, the Ca2+-dependent cascades are involved in GH secretion during the rebound phase but are not essential for the initiation of GnRH potentiation. Since GnRH has been previously shown to have no effects on cAMP synthesis in goldfish pituitary cells, the involvement of cAMP-dependent mechanisms in GnRH potentiation is rather unlikely. Copyright © 2007 the American Physiological Society.en_HK
dc.languageengen_HK
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://ajpendo.physiology.org/en_HK
dc.relation.ispartofAmerican Journal of Physiology - Endocrinology and Metabolismen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshDown-Regulationen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGene Expression - drug effectsen_HK
dc.subject.meshGoldfish - metabolismen_HK
dc.subject.meshGonadotropin-Releasing Hormone - pharmacologyen_HK
dc.subject.meshGrowth Hormone - metabolism - secretionen_HK
dc.subject.meshMaleen_HK
dc.subject.meshNorepinephrine - pharmacologyen_HK
dc.subject.meshPituitary Gland - metabolismen_HK
dc.subject.meshRNA, Messenger - metabolismen_HK
dc.titleMechanisms for gonadotropin-releasing hormone potentiation of growth hormone rebound following norepinephrine inhibition in goldfish pituitary cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0002-9513&volume=&spage=&epage=&date=2006&atitle=Mechanisms+for+gonadotropin-releasing+hormone+potentiation+of+growth+hormone+rebound+following+norepinephrine+inhibition+in+goldfish+pituitary+cellsen_HK
dc.identifier.emailWong, AOL: olwong@hkucc.hku.hken_HK
dc.identifier.authorityWong, AOL=rp00806en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1152/ajpendo.00337.2006en_HK
dc.identifier.pmid16940469-
dc.identifier.scopuseid_2-s2.0-33846052690en_HK
dc.identifier.hkuros123600en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33846052690&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume292en_HK
dc.identifier.issue1en_HK
dc.identifier.spageE203en_HK
dc.identifier.epageE214en_HK
dc.identifier.eissn1522-1555-
dc.identifier.isiWOS:000243253900027-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWong, AOL=7403147570en_HK
dc.identifier.scopusauthoridChuk, MCY=15759395500en_HK
dc.identifier.scopusauthoridHiu, CC=15759706500en_HK
dc.identifier.scopusauthoridLee, EKY=7406968652en_HK

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