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Article: Interactions of gonadal steroids with brain dopamine and gonadotropin- releasing hormone in the control of gonadotropin-II secretion in the goldfish

TitleInteractions of gonadal steroids with brain dopamine and gonadotropin- releasing hormone in the control of gonadotropin-II secretion in the goldfish
Authors
Issue Date1993
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ygcen
Citation
General And Comparative Endocrinology, 1993, v. 89 n. 1, p. 39-50 How to Cite?
AbstractIn goldfish it is known that intraperitoneal implantation with testosterone (T) or estradiol (E 2) potentiates the serum gonadotropin-II (GtH-II) response to gonadotropin-releasing hormone (GnRH) without affecting basal GtH-II levels. Since the release of GtH-II in goldfish is under a tonic dopaminergic inhibitory tone, the possibility of sex steroids modulating brain and pituitary dopamine was examined in vivo and in vitro. Implantation of females with either T or E 2 (100 μg/g in solid silastic pellets) also potentiated the increase in serum GtH-II in response to the dopamine antagonist, domperidone (10 μg/g). High-performance liquid chromatography measurements showed that steroid implantation had no effect on dopamine content in the telencephalon including preoptic area, hypothalamus, and pituitary. However, the present study demonstrates that T or E 2 can increase pituitary dopamine turnover rates following tyrosine hydroxylase inhibition with α-methyl-p-tyrosine (240 μg/g). In vitro perifusion of pars distalis fragments from E 2- or T-treated fish also showed a potentiation of salmon GnRH (sGnRH)-induced GtH-II release compared to controls. However, exposure to pituitary fragments from control and steroid-treated fish to increasing doses of the dopamine agonist LY 171555 did not demonstrate a significant difference in the sensitivity of the gonadotrophs to dopamine. Testosterone- induced alterations in DA turnover are dissociable from the positive action of T on pituitary responsiveness, since the potentiating effect of T implantation was not affected by severe depletion of brain and pituitary DA levels by α-methyl-p-tyrosine pretreatment. These data demonstrate that in gonad-intact goldfish, sex steroids enhance pituitary responsiveness to GnRH but basal serum GtH-II levels are maintained by a concomitant increase in DA turnover in the pituitary.
Persistent Identifierhttp://hdl.handle.net/10722/178552
ISSN
2015 Impact Factor: 2.667
2015 SCImago Journal Rankings: 1.245
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorTrudeau, VLen_US
dc.contributor.authorSloley, BDen_US
dc.contributor.authorWong, AOLen_US
dc.contributor.authorPeter, REen_US
dc.date.accessioned2012-12-19T09:48:20Z-
dc.date.available2012-12-19T09:48:20Z-
dc.date.issued1993en_US
dc.identifier.citationGeneral And Comparative Endocrinology, 1993, v. 89 n. 1, p. 39-50en_US
dc.identifier.issn0016-6480en_US
dc.identifier.urihttp://hdl.handle.net/10722/178552-
dc.description.abstractIn goldfish it is known that intraperitoneal implantation with testosterone (T) or estradiol (E 2) potentiates the serum gonadotropin-II (GtH-II) response to gonadotropin-releasing hormone (GnRH) without affecting basal GtH-II levels. Since the release of GtH-II in goldfish is under a tonic dopaminergic inhibitory tone, the possibility of sex steroids modulating brain and pituitary dopamine was examined in vivo and in vitro. Implantation of females with either T or E 2 (100 μg/g in solid silastic pellets) also potentiated the increase in serum GtH-II in response to the dopamine antagonist, domperidone (10 μg/g). High-performance liquid chromatography measurements showed that steroid implantation had no effect on dopamine content in the telencephalon including preoptic area, hypothalamus, and pituitary. However, the present study demonstrates that T or E 2 can increase pituitary dopamine turnover rates following tyrosine hydroxylase inhibition with α-methyl-p-tyrosine (240 μg/g). In vitro perifusion of pars distalis fragments from E 2- or T-treated fish also showed a potentiation of salmon GnRH (sGnRH)-induced GtH-II release compared to controls. However, exposure to pituitary fragments from control and steroid-treated fish to increasing doses of the dopamine agonist LY 171555 did not demonstrate a significant difference in the sensitivity of the gonadotrophs to dopamine. Testosterone- induced alterations in DA turnover are dissociable from the positive action of T on pituitary responsiveness, since the potentiating effect of T implantation was not affected by severe depletion of brain and pituitary DA levels by α-methyl-p-tyrosine pretreatment. These data demonstrate that in gonad-intact goldfish, sex steroids enhance pituitary responsiveness to GnRH but basal serum GtH-II levels are maintained by a concomitant increase in DA turnover in the pituitary.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.meshAnimalsen_US
dc.subject.meshBrain - Drug Effects - Metabolismen_US
dc.subject.meshChromatography, High Pressure Liquiden_US
dc.subject.meshDomperidone - Pharmacologyen_US
dc.subject.meshDopamine - Metabolismen_US
dc.subject.meshDrug Implantsen_US
dc.subject.meshEstradiol - Pharmacologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshGoldfish - Physiologyen_US
dc.subject.meshGonadotropin-Releasing Hormone - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshGonadotropins, Pituitary - Secretionen_US
dc.subject.meshPeritoneal Cavityen_US
dc.subject.meshPituitary Gland - Drug Effects - Metabolismen_US
dc.subject.meshTelencephalon - Drug Effects - Metabolismen_US
dc.subject.meshTestosterone - Pharmacologyen_US
dc.subject.meshTyrosine 3-Monooxygenase - Antagonists & Inhibitorsen_US
dc.titleInteractions of gonadal steroids with brain dopamine and gonadotropin- releasing hormone in the control of gonadotropin-II secretion 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.doi10.1006/gcen.1993.1007en_US
dc.identifier.pmid8094059-
dc.identifier.scopuseid_2-s2.0-0027470681en_US
dc.identifier.volume89en_US
dc.identifier.issue1en_US
dc.identifier.spage39en_US
dc.identifier.epage50en_US
dc.identifier.isiWOS:A1993KW63000006-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridTrudeau, VL=7006634572en_US
dc.identifier.scopusauthoridSloley, BD=7003269861en_US
dc.identifier.scopusauthoridWong, AOL=7403147570en_US
dc.identifier.scopusauthoridPeter, RE=7202909690en_US

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