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Article: Direct actions of serotonin on gonadotropin-II and growth hormone release from goldfish pituitary cells: Interactions with gonadotropin-releasing hormone and dopamine and further evaluation of serotonin receptor specificity

TitleDirect actions of serotonin on gonadotropin-II and growth hormone release from goldfish pituitary cells: Interactions with gonadotropin-releasing hormone and dopamine and further evaluation of serotonin receptor specificity
Authors
KeywordsDopamine
Goldfish
Gonadotropin
Gonadotropin-releasing hormone
Growth hormone
Pituitary cells
Serotonin
Serotonin receptors
Issue Date1998
PublisherSpringer Verlag Dordrecht. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0920-1742
Citation
Fish Physiology And Biochemistry, 1998, v. 19 n. 1, p. 23-34 How to Cite?
AbstractIn this study, the direct actions of serotonin (5HT) on gonadotropin (GTH)-II and growth hormone (GH) release in the goldfish were tested at the pituitary cell level. 5HT (10 nM - 10 μM) stimulated GTH-II but inhibited GH release from perifused goldfish pituitary cells in a dose-dependent manner. The minimal effective dose of 5HT tested to suppress basal GH secretion (10 nM) was 10-fold lower than that to stimulate GTH-II release (100 nM). The GTH-II releasing effect of 5HT was abolished by repeated 5HT treatment (10 μM) whereas the corresponding inhibition on GH release was unaffected. These results suggest that 5HT receptors on goldfish gonadotrophs and somatotrophs exhibit intrinsic differences in terms of sensitivity to stimulation and resistance to desensitization. Salmon GTH-releasing hormone (sGnRH, 100 nM) stimulated GTH-II and GH release from goldfish pituitary cells. The GTH-II releasing action of sGnRH was unaffected by simultaneous treatment of 5HT (1 μM). However, the corresponding GH response to sGnRH (100 nM) was inhibited. In the goldfish, dopamine is known to stimulate GH release through activation of pituitary D1 receptors. In the present study, the GH-releasing action of dopamine (1 μM) and the D1 agonist SKF38393 (1 μM) was significantly reduced by 5HT (1 μM). To examine the receptor specificity of 5HT action, the effects of 5HT1 and 5HT2 analogs on GTH-II and GH release were tested in goldfish pituitary cells. The 5HT1 agonist 8OH DPAT (0.1 and 1 μM) and 5HT2 agonist α methyl 5HT (0.1 1 μM) mimicked the GTH-II releasing effect of 5HT. The 5HT1 agonist 8OH DPAT (0.1 and 1 μM) also stimulated GH release but the 5HT2 agonist α methyl 5HT (0.1 and 1 μM) was inhibitory to basal GH secretion. In addition, 5HT (1 μM) -stimulated GTH-II release was abolished by the 5HT1 antagonist methiothepin (10 μM) and 5HT2 antagonist mianserin (10 μM). Similarly, the inhibitory action of 5HT (1 μM) on basal GH release was blocked by the 5HT2 antagonist mianserin (10 μM). The 5HT1 antagonist methiothepin (10 μM) was not effective in this regard. These results, taken together, indicate that 5HT exerts its regulatory actions on GTH-II and GH release in the goldfish directly at the pituitary cell level, probably through interactions with other regulators including sGnRH and dopamine. The GTH-II releasing action of 5HT is mediated through 5HT2 and possibly 5HT1 receptors. The inhibition of 5HT on basal GH release is mediated through 5HT2 receptors only. Apparently, 5HT1 receptors are not involved in this inhibitory action. In this study, a paradoxical stimulatory component of 5HT on GH release by activating 5HT1 receptors is also implicated.
Persistent Identifierhttp://hdl.handle.net/10722/84899
ISSN
2015 Impact Factor: 1.442
2015 SCImago Journal Rankings: 0.738
References

 

DC FieldValueLanguage
dc.contributor.authorWong, AOLen_HK
dc.contributor.authorMurphy, CKen_HK
dc.contributor.authorChang, JPen_HK
dc.contributor.authorNeumann, CMen_HK
dc.contributor.authorLo, Aen_HK
dc.contributor.authorPeter, REen_HK
dc.date.accessioned2010-09-06T08:58:25Z-
dc.date.available2010-09-06T08:58:25Z-
dc.date.issued1998en_HK
dc.identifier.citationFish Physiology And Biochemistry, 1998, v. 19 n. 1, p. 23-34en_HK
dc.identifier.issn0920-1742en_HK
dc.identifier.urihttp://hdl.handle.net/10722/84899-
dc.description.abstractIn this study, the direct actions of serotonin (5HT) on gonadotropin (GTH)-II and growth hormone (GH) release in the goldfish were tested at the pituitary cell level. 5HT (10 nM - 10 μM) stimulated GTH-II but inhibited GH release from perifused goldfish pituitary cells in a dose-dependent manner. The minimal effective dose of 5HT tested to suppress basal GH secretion (10 nM) was 10-fold lower than that to stimulate GTH-II release (100 nM). The GTH-II releasing effect of 5HT was abolished by repeated 5HT treatment (10 μM) whereas the corresponding inhibition on GH release was unaffected. These results suggest that 5HT receptors on goldfish gonadotrophs and somatotrophs exhibit intrinsic differences in terms of sensitivity to stimulation and resistance to desensitization. Salmon GTH-releasing hormone (sGnRH, 100 nM) stimulated GTH-II and GH release from goldfish pituitary cells. The GTH-II releasing action of sGnRH was unaffected by simultaneous treatment of 5HT (1 μM). However, the corresponding GH response to sGnRH (100 nM) was inhibited. In the goldfish, dopamine is known to stimulate GH release through activation of pituitary D1 receptors. In the present study, the GH-releasing action of dopamine (1 μM) and the D1 agonist SKF38393 (1 μM) was significantly reduced by 5HT (1 μM). To examine the receptor specificity of 5HT action, the effects of 5HT1 and 5HT2 analogs on GTH-II and GH release were tested in goldfish pituitary cells. The 5HT1 agonist 8OH DPAT (0.1 and 1 μM) and 5HT2 agonist α methyl 5HT (0.1 1 μM) mimicked the GTH-II releasing effect of 5HT. The 5HT1 agonist 8OH DPAT (0.1 and 1 μM) also stimulated GH release but the 5HT2 agonist α methyl 5HT (0.1 and 1 μM) was inhibitory to basal GH secretion. In addition, 5HT (1 μM) -stimulated GTH-II release was abolished by the 5HT1 antagonist methiothepin (10 μM) and 5HT2 antagonist mianserin (10 μM). Similarly, the inhibitory action of 5HT (1 μM) on basal GH release was blocked by the 5HT2 antagonist mianserin (10 μM). The 5HT1 antagonist methiothepin (10 μM) was not effective in this regard. These results, taken together, indicate that 5HT exerts its regulatory actions on GTH-II and GH release in the goldfish directly at the pituitary cell level, probably through interactions with other regulators including sGnRH and dopamine. The GTH-II releasing action of 5HT is mediated through 5HT2 and possibly 5HT1 receptors. The inhibition of 5HT on basal GH release is mediated through 5HT2 receptors only. Apparently, 5HT1 receptors are not involved in this inhibitory action. In this study, a paradoxical stimulatory component of 5HT on GH release by activating 5HT1 receptors is also implicated.en_HK
dc.languageengen_HK
dc.publisherSpringer Verlag Dordrecht. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0920-1742en_HK
dc.relation.ispartofFish Physiology and Biochemistryen_HK
dc.subjectDopamineen_HK
dc.subjectGoldfishen_HK
dc.subjectGonadotropinen_HK
dc.subjectGonadotropin-releasing hormoneen_HK
dc.subjectGrowth hormoneen_HK
dc.subjectPituitary cellsen_HK
dc.subjectSerotoninen_HK
dc.subjectSerotonin receptorsen_HK
dc.titleDirect actions of serotonin on gonadotropin-II and growth hormone release from goldfish pituitary cells: Interactions with gonadotropin-releasing hormone and dopamine and further evaluation of serotonin receptor specificityen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0920-1742&volume=19&spage=23&epage=24&date=1998&atitle=Direct+actions+of+serotonin+on+gonadotropin-II+and+growth+hormone+release+from+goldfish+pituitary+cells:-+Interactions+with+gonadotropin-releasing+hormone+and+dopamine+and+further+evaluation+of+serotonin+receptor+specificityen_HK
dc.identifier.emailWong, AOL: olwong@hkucc.hku.hken_HK
dc.identifier.authorityWong, AOL=rp00806en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.scopuseid_2-s2.0-0001974714en_HK
dc.identifier.hkuros36663en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0001974714&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume19en_HK
dc.identifier.issue1en_HK
dc.identifier.spage23en_HK
dc.identifier.epage34en_HK
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridWong, AOL=7403147570en_HK
dc.identifier.scopusauthoridMurphy, CK=7401763885en_HK
dc.identifier.scopusauthoridChang, JP=7601547649en_HK
dc.identifier.scopusauthoridNeumann, CM=16157956900en_HK
dc.identifier.scopusauthoridLo, A=8765899200en_HK
dc.identifier.scopusauthoridPeter, RE=7202909690en_HK

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