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Article: Relationship between cyclic AMP-stimulated and native gonadotropin- releasing hormone-stimulated gonadotropin release in the goldfish

TitleRelationship between cyclic AMP-stimulated and native gonadotropin- releasing hormone-stimulated gonadotropin release in the goldfish
Authors
Issue Date1992
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ygcen
Citation
General And Comparative Endocrinology, 1992, v. 86 n. 3, p. 359-377 How to Cite?
AbstractThe relationship between drugs elevating intracellular cAMP levels and gonadotropin (GTH)-releasing hormone (GnRH) in the stimulation of GTH secretion in the goldfish was investigated using dispersed goldfish pituitary cells in primary culture. In static incubation experiments, activation of adenylyl cyclase by forskolin and the inhibition of cAMP phosphodiesterase by 3 isobutyl-1-methylxanthine (IBMX) increased cAMP release and stimulated GTH secretion. The addition of membrane permeant cAMP analogs, 8-bromoadenosine 3':5'-cyclic monophosphate (8Br-cAMP), and dibutyryl cAMP also increased GTH release, suggesting that elevation of cAMP levels can induce GTH secretion. In the goldfish, dopamine is a physiological inhibitor of GTH release. Application of the dopamine agonist apomorphine decreased the GTH responses to forskolin, 8Br-cAMP, and salmon GTH-releasing hormone (sGnRH). The ability of agents that elevate cAMP levels to mimic GnRH action on GTH release suggests that cAMP may mediate GnRH-stimulated GTH secretion in the goldfish; however, this possibility was not substantiated by results from further experiments. In 2-hr static incubation studies, the GTH responses to sGnRH and chicken GnRH-II (cGnRH-II) were enhanced by coincubations with forskolin, IBMX, and 8Br-cAMP. The magnitudes of these enhancements were at least additive, if not synergistic. The levels of cAMP released into the media were unaffected by treatment with sGnRH and cGnRH-II, either in the absence or in the presence of IBMX. Replacement of normal testing media with Ca 2+- deficient media (without Ca 2+ salts and in the presence of 0.1 mM EGTA) decreased sGnRH and cGnRH-II stimulation of GTH release but did not affect forskolin and 8Br-cAMP actions. These results indicate that sGnRH and cGnRH- II stimulation of short term (≤2-h) GTH release in the goldfish is not mediated by cAMP. The kinetics of the interactions between sGnRH, forskolin, and IBMX were also investigated in cell column perifusion studies. Applications of 5-min pulses of forskolin and IBMX stimulated rapid increases in GTH release; the latencies of these responses were similar to that observed with sGnRH. The simultaneous applications of sGnRH with either forskolin or IBMX resulted in GTH responses that were of greater magnitude and longer duration than those in response to sGnRH alone. These results together indicate that elevation of cAMP levels can potentiate the GTH response to the native GnRHs by increasing the magnitude of the acute GTH release and by prolonging the duration of GnRH action; however, cAMP does not appear to be involved directly in mediating GnRH stimulation of GTH release. It is possible that some unknown neuroendocrine regulator elevates cAMP to positively modulate GnRH actions on GTH release in the goldfish.
Persistent Identifierhttp://hdl.handle.net/10722/178530
ISSN
2015 Impact Factor: 2.667
2015 SCImago Journal Rankings: 1.245
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChang, JPen_US
dc.contributor.authorWong, AOLen_US
dc.contributor.authorVan Der Kraak, Gen_US
dc.contributor.authorVan Goor, Fen_US
dc.date.accessioned2012-12-19T09:48:15Z-
dc.date.available2012-12-19T09:48:15Z-
dc.date.issued1992en_US
dc.identifier.citationGeneral And Comparative Endocrinology, 1992, v. 86 n. 3, p. 359-377en_US
dc.identifier.issn0016-6480en_US
dc.identifier.urihttp://hdl.handle.net/10722/178530-
dc.description.abstractThe relationship between drugs elevating intracellular cAMP levels and gonadotropin (GTH)-releasing hormone (GnRH) in the stimulation of GTH secretion in the goldfish was investigated using dispersed goldfish pituitary cells in primary culture. In static incubation experiments, activation of adenylyl cyclase by forskolin and the inhibition of cAMP phosphodiesterase by 3 isobutyl-1-methylxanthine (IBMX) increased cAMP release and stimulated GTH secretion. The addition of membrane permeant cAMP analogs, 8-bromoadenosine 3':5'-cyclic monophosphate (8Br-cAMP), and dibutyryl cAMP also increased GTH release, suggesting that elevation of cAMP levels can induce GTH secretion. In the goldfish, dopamine is a physiological inhibitor of GTH release. Application of the dopamine agonist apomorphine decreased the GTH responses to forskolin, 8Br-cAMP, and salmon GTH-releasing hormone (sGnRH). The ability of agents that elevate cAMP levels to mimic GnRH action on GTH release suggests that cAMP may mediate GnRH-stimulated GTH secretion in the goldfish; however, this possibility was not substantiated by results from further experiments. In 2-hr static incubation studies, the GTH responses to sGnRH and chicken GnRH-II (cGnRH-II) were enhanced by coincubations with forskolin, IBMX, and 8Br-cAMP. The magnitudes of these enhancements were at least additive, if not synergistic. The levels of cAMP released into the media were unaffected by treatment with sGnRH and cGnRH-II, either in the absence or in the presence of IBMX. Replacement of normal testing media with Ca 2+- deficient media (without Ca 2+ salts and in the presence of 0.1 mM EGTA) decreased sGnRH and cGnRH-II stimulation of GTH release but did not affect forskolin and 8Br-cAMP actions. These results indicate that sGnRH and cGnRH- II stimulation of short term (≤2-h) GTH release in the goldfish is not mediated by cAMP. The kinetics of the interactions between sGnRH, forskolin, and IBMX were also investigated in cell column perifusion studies. Applications of 5-min pulses of forskolin and IBMX stimulated rapid increases in GTH release; the latencies of these responses were similar to that observed with sGnRH. The simultaneous applications of sGnRH with either forskolin or IBMX resulted in GTH responses that were of greater magnitude and longer duration than those in response to sGnRH alone. These results together indicate that elevation of cAMP levels can potentiate the GTH response to the native GnRHs by increasing the magnitude of the acute GTH release and by prolonging the duration of GnRH action; however, cAMP does not appear to be involved directly in mediating GnRH stimulation of GTH release. It is possible that some unknown neuroendocrine regulator elevates cAMP to positively modulate GnRH actions on GTH release in the goldfish.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.mesh1-Methyl-3-Isobutylxanthine - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCalcium - Physiologyen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCyclic Amp - Analogs & Derivatives - Metabolism - Pharmacologyen_US
dc.subject.meshDopamine Agents - Pharmacologyen_US
dc.subject.meshForskolin - Pharmacologyen_US
dc.subject.meshGoldfish - Metabolismen_US
dc.subject.meshGonadotropin-Releasing Hormone - Pharmacologyen_US
dc.subject.meshGonadotropins - Metabolismen_US
dc.subject.meshKineticsen_US
dc.subject.meshNerve Endings - Drug Effects - Metabolismen_US
dc.titleRelationship between cyclic AMP-stimulated and native gonadotropin- releasing hormone-stimulated gonadotropin release in the goldfishen_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.doi10.1016/0016-6480(92)90061-Nen_US
dc.identifier.pmid1383076-
dc.identifier.scopuseid_2-s2.0-0026654575en_US
dc.identifier.volume86en_US
dc.identifier.issue3en_US
dc.identifier.spage359en_US
dc.identifier.epage377en_US
dc.identifier.isiWOS:A1992HV41600004-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridChang, JP=7601547649en_US
dc.identifier.scopusauthoridWong, AOL=7403147570en_US
dc.identifier.scopusauthoridVan der Kraak, G=35601666000en_US
dc.identifier.scopusauthoridVan Goor, F=35845505200en_US

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