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Growth Hormone Secretagogue Activation of the Arcuate Nucleus and Brainstem Occurs Via a Non-Noradrenergic Pathway
Noradrenergic systems are integrally involved in the release of growth hormone (GH) from the anterior pituitary gland and in regulating the activity of hypothalamic growth hormone‐releasing hormone (GHRH) neurones. GH secretagogues act at both the pituitary and the hypothalamus to facilitate the rel...
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Published in: | Journal of neuroendocrinology 2000-03, Vol.12 (3), p.191-197 |
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creator | Bailey, A R von Engelhardt, N Von Englehardt, N Leng, G Smith, R G Dickson, S L |
description | Noradrenergic systems are integrally involved in the release of growth hormone (GH) from the anterior pituitary gland and in regulating the activity of hypothalamic growth hormone‐releasing hormone (GHRH) neurones. GH secretagogues act at both the pituitary and the hypothalamus to facilitate the release of GH. In male rats, using the induction of Fos protein as an indicator of neuronal activation, we examined whether neurones in the brainstem, the main noradrenergic input to the hypothalamus, were activated by systemic administration of peptide and non‐peptide GH secretagogues. In addition, we examined the effects of chronic central noradrenaline depletion upon GH secretagogue‐induced activation of the arcuate nucleus. Systemic injection of the GH secretagogues, GHRP‐6 and MK‐0677 induced Fos protein expression in a population of area postrema cells, but less than 10% of these cells were noradrenergic. Depletion of hypothalamic noradrenaline by the specific neurotoxin, 5‐ADMP, did not alter GH secretagogue‐induced activation of Fos protein in the arcuate nucleus compared to vehicle‐treated controls. We conclude that the central actions of GH secretagogues involve the activation of non‐noradrenergic cells in the area postrema and that GH secretagogue‐induced activation of the arcuate nucleus occurs independently of noradrenergic tone. |
doi_str_mv | 10.1046/j.1365-2826.2000.00398.x |
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GH secretagogues act at both the pituitary and the hypothalamus to facilitate the release of GH. In male rats, using the induction of Fos protein as an indicator of neuronal activation, we examined whether neurones in the brainstem, the main noradrenergic input to the hypothalamus, were activated by systemic administration of peptide and non‐peptide GH secretagogues. In addition, we examined the effects of chronic central noradrenaline depletion upon GH secretagogue‐induced activation of the arcuate nucleus. Systemic injection of the GH secretagogues, GHRP‐6 and MK‐0677 induced Fos protein expression in a population of area postrema cells, but less than 10% of these cells were noradrenergic. Depletion of hypothalamic noradrenaline by the specific neurotoxin, 5‐ADMP, did not alter GH secretagogue‐induced activation of Fos protein in the arcuate nucleus compared to vehicle‐treated controls. We conclude that the central actions of GH secretagogues involve the activation of non‐noradrenergic cells in the area postrema and that GH secretagogue‐induced activation of the arcuate nucleus occurs independently of noradrenergic tone.</description><identifier>ISSN: 0953-8194</identifier><identifier>EISSN: 1365-2826</identifier><identifier>DOI: 10.1046/j.1365-2826.2000.00398.x</identifier><identifier>PMID: 10718914</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Animals ; Arcuate Nucleus of Hypothalamus - chemistry ; Arcuate Nucleus of Hypothalamus - drug effects ; Arcuate Nucleus of Hypothalamus - physiology ; area postrema ; Brain Stem - chemistry ; Brain Stem - drug effects ; Brain Stem - physiology ; GHRP-6 ; Growth Hormone - secretion ; growth hormone secretagogues ; Growth Hormone-Releasing Hormone - pharmacology ; Indoles - pharmacology ; Male ; Neurotoxins - pharmacology ; noradrenaline ; Oligopeptides - pharmacology ; Phenethylamines - pharmacology ; Proto-Oncogene Proteins c-fos - analysis ; Rats ; Rats, Sprague-Dawley ; Spiro Compounds - pharmacology ; Tyrosine 3-Monooxygenase - analysis</subject><ispartof>Journal of neuroendocrinology, 2000-03, Vol.12 (3), p.191-197</ispartof><rights>Copyright Blackwell Scientific Publications Ltd. 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von Engelhardt, N ; Von Englehardt, N ; Leng, G ; Smith, R G ; Dickson, S L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4958-366c06410861b21c7d6f20347ffca60ab8ed44dce57d4793b6a7af480be6fbad3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Animals</topic><topic>Arcuate Nucleus of Hypothalamus - chemistry</topic><topic>Arcuate Nucleus of Hypothalamus - drug effects</topic><topic>Arcuate Nucleus of Hypothalamus - physiology</topic><topic>area postrema</topic><topic>Brain Stem - chemistry</topic><topic>Brain Stem - drug effects</topic><topic>Brain Stem - physiology</topic><topic>GHRP-6</topic><topic>Growth Hormone - secretion</topic><topic>growth hormone secretagogues</topic><topic>Growth Hormone-Releasing Hormone - pharmacology</topic><topic>Indoles - pharmacology</topic><topic>Male</topic><topic>Neurotoxins - pharmacology</topic><topic>noradrenaline</topic><topic>Oligopeptides - pharmacology</topic><topic>Phenethylamines - pharmacology</topic><topic>Proto-Oncogene Proteins c-fos - analysis</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Spiro Compounds - pharmacology</topic><topic>Tyrosine 3-Monooxygenase - analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bailey, A R</creatorcontrib><creatorcontrib>von Engelhardt, N</creatorcontrib><creatorcontrib>Von Englehardt, N</creatorcontrib><creatorcontrib>Leng, G</creatorcontrib><creatorcontrib>Smith, R G</creatorcontrib><creatorcontrib>Dickson, S L</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>Journal of neuroendocrinology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bailey, A R</au><au>von Engelhardt, N</au><au>Von Englehardt, N</au><au>Leng, G</au><au>Smith, R G</au><au>Dickson, S L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Growth Hormone Secretagogue Activation of the Arcuate Nucleus and Brainstem Occurs Via a Non-Noradrenergic Pathway</atitle><jtitle>Journal of neuroendocrinology</jtitle><addtitle>Journal of Neuroendocrinology</addtitle><date>2000-03</date><risdate>2000</risdate><volume>12</volume><issue>3</issue><spage>191</spage><epage>197</epage><pages>191-197</pages><issn>0953-8194</issn><eissn>1365-2826</eissn><abstract>Noradrenergic systems are integrally involved in the release of growth hormone (GH) from the anterior pituitary gland and in regulating the activity of hypothalamic growth hormone‐releasing hormone (GHRH) neurones. GH secretagogues act at both the pituitary and the hypothalamus to facilitate the release of GH. In male rats, using the induction of Fos protein as an indicator of neuronal activation, we examined whether neurones in the brainstem, the main noradrenergic input to the hypothalamus, were activated by systemic administration of peptide and non‐peptide GH secretagogues. In addition, we examined the effects of chronic central noradrenaline depletion upon GH secretagogue‐induced activation of the arcuate nucleus. Systemic injection of the GH secretagogues, GHRP‐6 and MK‐0677 induced Fos protein expression in a population of area postrema cells, but less than 10% of these cells were noradrenergic. Depletion of hypothalamic noradrenaline by the specific neurotoxin, 5‐ADMP, did not alter GH secretagogue‐induced activation of Fos protein in the arcuate nucleus compared to vehicle‐treated controls. We conclude that the central actions of GH secretagogues involve the activation of non‐noradrenergic cells in the area postrema and that GH secretagogue‐induced activation of the arcuate nucleus occurs independently of noradrenergic tone.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>10718914</pmid><doi>10.1046/j.1365-2826.2000.00398.x</doi><tpages>7</tpages></addata></record> |
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subjects | Animals Arcuate Nucleus of Hypothalamus - chemistry Arcuate Nucleus of Hypothalamus - drug effects Arcuate Nucleus of Hypothalamus - physiology area postrema Brain Stem - chemistry Brain Stem - drug effects Brain Stem - physiology GHRP-6 Growth Hormone - secretion growth hormone secretagogues Growth Hormone-Releasing Hormone - pharmacology Indoles - pharmacology Male Neurotoxins - pharmacology noradrenaline Oligopeptides - pharmacology Phenethylamines - pharmacology Proto-Oncogene Proteins c-fos - analysis Rats Rats, Sprague-Dawley Spiro Compounds - pharmacology Tyrosine 3-Monooxygenase - analysis |
title | Growth Hormone Secretagogue Activation of the Arcuate Nucleus and Brainstem Occurs Via a Non-Noradrenergic Pathway |
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