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Article: Neuropeptide-Y stimulates growth hormone and gonadotropin-II secretion in the goldfish pituitary: Involvement of both presynaptic and pituitary cell actions

TitleNeuropeptide-Y stimulates growth hormone and gonadotropin-II secretion in the goldfish pituitary: Involvement of both presynaptic and pituitary cell actions
Authors
Issue Date1993
PublisherThe Endocrine Society. The Journal's web site is located at http://endo.endojournals.org
Citation
Endocrinology, 1993, v. 132 n. 4, p. 1820-1829 How to Cite?
AbstractWe have previously reported that neuropeptide-Y (NPY) stimulates GH and gonadotropin-II (GtH-II) release from perifused pituitary fragments in the goldfish. Since the teleost pituitary is directly innervated by neurosecretory terminals from the brain, we further investigated the possible sites of action of NPY. Both synthetic human NPY and NPY-(18-36), an agonist selective for the NPY Y2-receptor, stimulated GH and GtH-II release from the pituitary fragments; the magnitude of the response to NPY (18-36) was smaller than that to the whole molecule of NPY. NPY also stimulated the release of GH and GtH-II from perifused dispersed pituitary cells. In contrast, NPY-(18- 36) had no effect on either GH or GtH-II release from dispersed pituitary cells. These data suggest that Y2 action is not direct at the level of pituitary cells, but may be indirect through actions on nerve terminals in the pituitary. The hypothesis that the action of NPY on GH and GtH-II release is mediated in part by GnRH was then tested. Both NPY and NPY-(18-36) stimulated the GnRH release from preoptic-anterior hypothalamic slices and pituitary fragments with similar potency. Furthermore, a GnRH antagonist significantly reduced the effects of NPY on both GH and GtH-II release in perifused pituitary fragments. Similar to previous findings, NPY, when given at 55-min intervals, desensitized the hormone responses in pituitary fragments. Similarly, the same treatment with NPY in perifused dispersed pituitary cells induced desensitization of GH and GtH-II responses. Together, these results suggest that 1) more than one type of NPY receptors are present in the goldfish pituitary; and 2) NPY has at least two sites of action in the pituitary. One site of action is the pituitary cells, where NPY directly stimulates GH and GtH-II secretion; the second is the nerve terminals, where NPY presynaptically stimulates GnRH release via Y2-like receptors, and GnRH, in turn, stimulates GH and GtH-II release.
Persistent Identifierhttp://hdl.handle.net/10722/178549
ISSN
2015 Impact Factor: 4.159
2015 SCImago Journal Rankings: 2.363
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorPeng, Cen_US
dc.contributor.authorChang, JPen_US
dc.contributor.authorKei Li Yuen_US
dc.contributor.authorWong, AOLen_US
dc.contributor.authorVan Goor, Fen_US
dc.contributor.authorPeter, REen_US
dc.contributor.authorRivier, JEen_US
dc.date.accessioned2012-12-19T09:48:19Z-
dc.date.available2012-12-19T09:48:19Z-
dc.date.issued1993en_US
dc.identifier.citationEndocrinology, 1993, v. 132 n. 4, p. 1820-1829en_US
dc.identifier.issn0013-7227en_US
dc.identifier.urihttp://hdl.handle.net/10722/178549-
dc.description.abstractWe have previously reported that neuropeptide-Y (NPY) stimulates GH and gonadotropin-II (GtH-II) release from perifused pituitary fragments in the goldfish. Since the teleost pituitary is directly innervated by neurosecretory terminals from the brain, we further investigated the possible sites of action of NPY. Both synthetic human NPY and NPY-(18-36), an agonist selective for the NPY Y2-receptor, stimulated GH and GtH-II release from the pituitary fragments; the magnitude of the response to NPY (18-36) was smaller than that to the whole molecule of NPY. NPY also stimulated the release of GH and GtH-II from perifused dispersed pituitary cells. In contrast, NPY-(18- 36) had no effect on either GH or GtH-II release from dispersed pituitary cells. These data suggest that Y2 action is not direct at the level of pituitary cells, but may be indirect through actions on nerve terminals in the pituitary. The hypothesis that the action of NPY on GH and GtH-II release is mediated in part by GnRH was then tested. Both NPY and NPY-(18-36) stimulated the GnRH release from preoptic-anterior hypothalamic slices and pituitary fragments with similar potency. Furthermore, a GnRH antagonist significantly reduced the effects of NPY on both GH and GtH-II release in perifused pituitary fragments. Similar to previous findings, NPY, when given at 55-min intervals, desensitized the hormone responses in pituitary fragments. Similarly, the same treatment with NPY in perifused dispersed pituitary cells induced desensitization of GH and GtH-II responses. Together, these results suggest that 1) more than one type of NPY receptors are present in the goldfish pituitary; and 2) NPY has at least two sites of action in the pituitary. One site of action is the pituitary cells, where NPY directly stimulates GH and GtH-II secretion; the second is the nerve terminals, where NPY presynaptically stimulates GnRH release via Y2-like receptors, and GnRH, in turn, stimulates GH and GtH-II release.en_US
dc.languageengen_US
dc.publisherThe Endocrine Society. The Journal's web site is located at http://endo.endojournals.orgen_US
dc.relation.ispartofEndocrinologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshDrug Interactionsen_US
dc.subject.meshFemaleen_US
dc.subject.meshGoldfishen_US
dc.subject.meshGonadotropin-Releasing Hormone - Antagonists & Inhibitorsen_US
dc.subject.meshGonadotropins, Pituitary - Secretionen_US
dc.subject.meshGrowth Hormone - Secretionen_US
dc.subject.meshHypothalamus, Anterior - Metabolismen_US
dc.subject.meshNeuropeptide Y - Metabolism - Pharmacologyen_US
dc.subject.meshPeptide Fragments - Pharmacologyen_US
dc.subject.meshPituitary Gland - Cytology - Metabolism - Physiologyen_US
dc.subject.meshSynapses - Physiologyen_US
dc.titleNeuropeptide-Y stimulates growth hormone and gonadotropin-II secretion in the goldfish pituitary: Involvement of both presynaptic and pituitary cell actionsen_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.doi10.1210/en.132.4.1820en_US
dc.identifier.pmid8462479-
dc.identifier.scopuseid_2-s2.0-0027401981en_US
dc.identifier.volume132en_US
dc.identifier.issue4en_US
dc.identifier.spage1820en_US
dc.identifier.epage1829en_US
dc.identifier.isiWOS:A1993KV62900055-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridPeng, C=7401797928en_US
dc.identifier.scopusauthoridChang, JP=7601547649en_US
dc.identifier.scopusauthoridKei Li Yu=7409802262en_US
dc.identifier.scopusauthoridWong, AOL=7403147570en_US
dc.identifier.scopusauthoridVan Goor, F=35845505200en_US
dc.identifier.scopusauthoridPeter, RE=7202909690en_US
dc.identifier.scopusauthoridRivier, JE=35411857000en_US

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