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Article: Dexamethasone decreases somatostatin mRNA levels in the periventricular nucleus of the rat hypothalamus

TitleDexamethasone decreases somatostatin mRNA levels in the periventricular nucleus of the rat hypothalamus
Authors
KeywordsDexamethasone
Gene expression
Glucocorticoid
Hypothalamus
In situ hybridization
Periventricular nucleus
Somatostatin
Issue Date1993
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/NEN
Citation
Neuroendocrinology, 1993, v. 58 n. 3, p. 325-331 How to Cite?
AbstractGlucocorticoid excess inhibits somatic growth in man and laboratory animals. While the mechanism involved is likely to be multifactorial, indirect evidence suggesting the role of an enhanced endogenous somatostatin (SS) tone has been reported. However, there has been no direct evidence indicating an increased synthesis or secretion of hypothalamic SS. In this study, we investigated the effects of glucocorticoids on hypothalamic SS expression by measuring the peptide and mRNA content of SS in whole hypothalamic blocks of male Sprague-Dawley rats sacrificed 4 weeks after adrenalectomy or sham operation. Adrenalectomy decreased the SS content in the rat hypothalamus (p < 0.05), an effect which was reversed by dexamethasone treatment for 10 days. On the other hand, total hypothalamic SS mRNA levels were unaffected by adrenalectomy, but became significantly decreased following dexamethasone treatment (p < 0.05). Using in situ hybridization, this reduction in SS gene expression was shown to occur consistently in the periventricular nucleus and in the parvocellular subdivision of the paraventricular nucleus. The effects of adrenalectomy and dexamethasone on SS mRNA levels were further quantitated in hypothalamic fragments containing predominantly the periventricular and paraventricular nuclei. Somatostatin mRNA levels in these tissue fragments were marginally increased by adrenalectomy (p < 0.05), but showed a 50% reduction following dexamethasone treatment (p < 0.0001). In conclusion, our findings suggest that the inhibitory effect of glucocorticoids on somatic growth is probably not mediated via an effect on hypothalamic SS gene expression.
Persistent Identifierhttp://hdl.handle.net/10722/146620
ISSN
2023 Impact Factor: 3.2
2023 SCImago Journal Rankings: 1.009
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLam, KSLen_HK
dc.contributor.authorSrivastava, Gen_HK
dc.contributor.authorTam, SPen_HK
dc.contributor.authorChung, LPen_HK
dc.contributor.authorChan, SFen_HK
dc.contributor.authorTang, Fen_HK
dc.contributor.authorChung, SKen_HK
dc.date.accessioned2012-05-08T03:21:19Z-
dc.date.available2012-05-08T03:21:19Z-
dc.date.issued1993en_HK
dc.identifier.citationNeuroendocrinology, 1993, v. 58 n. 3, p. 325-331en_HK
dc.identifier.issn0028-3835en_HK
dc.identifier.urihttp://hdl.handle.net/10722/146620-
dc.description.abstractGlucocorticoid excess inhibits somatic growth in man and laboratory animals. While the mechanism involved is likely to be multifactorial, indirect evidence suggesting the role of an enhanced endogenous somatostatin (SS) tone has been reported. However, there has been no direct evidence indicating an increased synthesis or secretion of hypothalamic SS. In this study, we investigated the effects of glucocorticoids on hypothalamic SS expression by measuring the peptide and mRNA content of SS in whole hypothalamic blocks of male Sprague-Dawley rats sacrificed 4 weeks after adrenalectomy or sham operation. Adrenalectomy decreased the SS content in the rat hypothalamus (p < 0.05), an effect which was reversed by dexamethasone treatment for 10 days. On the other hand, total hypothalamic SS mRNA levels were unaffected by adrenalectomy, but became significantly decreased following dexamethasone treatment (p < 0.05). Using in situ hybridization, this reduction in SS gene expression was shown to occur consistently in the periventricular nucleus and in the parvocellular subdivision of the paraventricular nucleus. The effects of adrenalectomy and dexamethasone on SS mRNA levels were further quantitated in hypothalamic fragments containing predominantly the periventricular and paraventricular nuclei. Somatostatin mRNA levels in these tissue fragments were marginally increased by adrenalectomy (p < 0.05), but showed a 50% reduction following dexamethasone treatment (p < 0.0001). In conclusion, our findings suggest that the inhibitory effect of glucocorticoids on somatic growth is probably not mediated via an effect on hypothalamic SS gene expression.en_HK
dc.languageengen_US
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/NENen_HK
dc.relation.ispartofNeuroendocrinologyen_HK
dc.subjectDexamethasoneen_HK
dc.subjectGene expressionen_HK
dc.subjectGlucocorticoiden_HK
dc.subjectHypothalamusen_HK
dc.subjectIn situ hybridizationen_HK
dc.subjectPeriventricular nucleusen_HK
dc.subjectSomatostatinen_HK
dc.subject.meshAdrenalectomyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBody Weight - Drug Effectsen_US
dc.subject.meshDexamethasone - Pharmacologyen_US
dc.subject.meshGrowth Hormone - Blood - Metabolismen_US
dc.subject.meshHypothalamus - Drug Effects - Metabolismen_US
dc.subject.meshIn Situ Hybridizationen_US
dc.subject.meshMaleen_US
dc.subject.meshParaventricular Hypothalamic Nucleus - Drug Effects - Metabolismen_US
dc.subject.meshRna, Messenger - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshSomatostatin - Geneticsen_US
dc.titleDexamethasone decreases somatostatin mRNA levels in the periventricular nucleus of the rat hypothalamusen_HK
dc.typeArticleen_HK
dc.identifier.emailLam, KSL: ksllam@hku.hken_HK
dc.identifier.emailSrivastava, G: sgopesh@hkucc.hku.hken_HK
dc.identifier.emailChung, LP: lpchung@hkucc.hku.hken_HK
dc.identifier.emailTang, F: ftang@hkucc.hku.hken_HK
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_HK
dc.identifier.authorityLam, KSL=rp00343en_HK
dc.identifier.authoritySrivastava, G=rp00365en_HK
dc.identifier.authorityChung, LP=rp00249en_HK
dc.identifier.authorityTang, F=rp00327en_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1159/000126557-
dc.identifier.pmid7902961-
dc.identifier.scopuseid_2-s2.0-0027484952en_HK
dc.identifier.volume58en_HK
dc.identifier.issue3en_HK
dc.identifier.spage325en_HK
dc.identifier.epage331en_HK
dc.identifier.isiWOS:A1993ME44200008-
dc.publisher.placeSwitzerlanden_HK
dc.identifier.scopusauthoridLam, KSL=8082870600en_HK
dc.identifier.scopusauthoridSrivastava, G=7202242238en_HK
dc.identifier.scopusauthoridTam, SP=7202036931en_HK
dc.identifier.scopusauthoridChung, LP=24315879100en_HK
dc.identifier.scopusauthoridChan, SF=7404255229en_HK
dc.identifier.scopusauthoridTang, F=7201979770en_HK
dc.identifier.scopusauthoridChung, SK=7404292976en_HK
dc.identifier.issnl0028-3835-

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