Pavlovian conditioning of corticotropin‐releasing factor‐induced increase of blood pressure and corticosterone secretion in the rat
Identifieur interne : 000B74 ( Istex/Corpus ); précédent : 000B73; suivant : 000B75Pavlovian conditioning of corticotropin‐releasing factor‐induced increase of blood pressure and corticosterone secretion in the rat
Auteurs : M. Kreutz ; D. Hellhammer ; R. Murison ; H. Vetter ; U. Krause ; H. LehnertSource :
- Acta Physiologica Scandinavica [ 0001-6772 ] ; 1992-05.
English descriptors
Abstract
Corticotropin‐releasing factor (CRF) is clearly involved in the central regulation of the pituitary‐adrenal axis and, moreover, of autonomic nervous system functions. Enhanced sympathetic activity with subsequent increases in blood pressure and heart rate and attenuation of the baroreceptor reflex results from the intracerebroventricular (i.c.v.) administration of CRF. Additionally, the peptide has a variety of potent effects on behavioural responses in animals similar to those observed after an experimentally evoked stress. It was therefore of obvious interest to examine whether CRF is a possible mediator of the learning processes associated with physiological stress reaction patterns. This report clearly demonstrates a classical conditioning of the endocrine (i.e. corticosterone secretion) and haemodynamic (i.e. blood pressure) sequelae following central CRF application and thus indicates that this mechanism is of physiological significance for learned stress responses.
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DOI: 10.1111/j.1748-1716.1992.tb09336.x
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Kreutz</name><affiliation><mods:affiliation>Department of Molecular Neuroendocrinology, Max‐Planck‐Institute of Experimental Medicine, Göttingen, FRG</mods:affiliation></affiliation></author><author><name sortKey="Hellhammer, D" sort="Hellhammer, D" uniqKey="Hellhammer D" first="D." last="Hellhammer">D. Hellhammer</name><affiliation><mods:affiliation>Department of Physiological and Clinical Psychology, University of Trier, Trier‐Tarforst, Germany</mods:affiliation></affiliation></author><author><name sortKey="Murison, R" sort="Murison, R" uniqKey="Murison R" first="R." last="Murison">R. Murison</name><affiliation><mods:affiliation>Department of Physiological Psychology, University of Bergen, Bergen, Norway</mods:affiliation></affiliation></author><author><name sortKey="Vetter, H" sort="Vetter, H" uniqKey="Vetter H" first="H." last="Vetter">H. Vetter</name><affiliation><mods:affiliation>Department of Internal Medicine (Medizinische Poliklinik), Bonn, Germany</mods:affiliation></affiliation></author><author><name sortKey="Krause, U" sort="Krause, U" uniqKey="Krause U" first="U." last="Krause">U. Krause</name><affiliation><mods:affiliation>Department of Internal Medicine‐ Endocrinology and Metabolism, University of Mainz, Mainz, Germany</mods:affiliation></affiliation></author><author><name sortKey="Lehnert, H" sort="Lehnert, H" uniqKey="Lehnert H" first="H." last="Lehnert">H. Lehnert</name><affiliation><mods:affiliation>Department of Internal Medicine‐ Endocrinology and Metabolism, University of Mainz, Mainz, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Internal Medicine (Endocrinology and Metabolism), University of Mainz, Langenbeckstrasse 1, 6500 Mainz, Germany.</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Acta Physiologica Scandinavica</title><idno type="ISSN">0001-6772</idno><idno type="eISSN">1365-201X</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1992-05">1992-05</date><biblScope unit="volume">145</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="59">59</biblScope><biblScope unit="page" to="63">63</biblScope></imprint><idno type="ISSN">0001-6772</idno></series><idno type="istex">953AA63343A9B048E07CE68CE9682C9F163A19F4</idno><idno type="DOI">10.1111/j.1748-1716.1992.tb09336.x</idno><idno type="ArticleID">APHA59</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0001-6772</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>blood pressure</term><term>classical conditioning</term><term>corticosterone</term><term>corticotropinreleasing factor.</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Corticotropin‐releasing factor (CRF) is clearly involved in the central regulation of the pituitary‐adrenal axis and, moreover, of autonomic nervous system functions. Enhanced sympathetic activity with subsequent increases in blood pressure and heart rate and attenuation of the baroreceptor reflex results from the intracerebroventricular (i.c.v.) administration of CRF. Additionally, the peptide has a variety of potent effects on behavioural responses in animals similar to those observed after an experimentally evoked stress. It was therefore of obvious interest to examine whether CRF is a possible mediator of the learning processes associated with physiological stress reaction patterns. This report clearly demonstrates a classical conditioning of the endocrine (i.e. corticosterone secretion) and haemodynamic (i.e. blood pressure) sequelae following central CRF application and thus indicates that this mechanism is of physiological significance for learned stress responses.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>M. KREUTZ</name><affiliations><json:string>Department of Molecular Neuroendocrinology, Max‐Planck‐Institute of Experimental Medicine, Göttingen, FRG</json:string></affiliations></json:item><json:item><name>D. HELLHAMMER</name><affiliations><json:string>Department of Physiological and Clinical Psychology, University of Trier, Trier‐Tarforst, Germany</json:string></affiliations></json:item><json:item><name>R. MURISON</name><affiliations><json:string>Department of Physiological Psychology, University of Bergen, Bergen, Norway</json:string></affiliations></json:item><json:item><name>H. VETTER</name><affiliations><json:string>Department of Internal Medicine (Medizinische Poliklinik), Bonn, Germany</json:string></affiliations></json:item><json:item><name>U. KRAUSE</name><affiliations><json:string>Department of Internal Medicine‐ Endocrinology and Metabolism, University of Mainz, Mainz, Germany</json:string></affiliations></json:item><json:item><name>H. LEHNERT</name><affiliations><json:string>Department of Internal Medicine‐ Endocrinology and Metabolism, University of Mainz, Mainz, Germany</json:string><json:string>Department of Internal Medicine (Endocrinology and Metabolism), University of Mainz, Langenbeckstrasse 1, 6500 Mainz, Germany.</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>blood pressure</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>classical conditioning</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>corticosterone</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>corticotropinreleasing factor.</value></json:item></subject><articleId><json:string>APHA59</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Corticotropin‐releasing factor (CRF) is clearly involved in the central regulation of the pituitary‐adrenal axis and, moreover, of autonomic nervous system functions. 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This report clearly demonstrates a classical conditioning of the endocrine (i.e. corticosterone secretion) and haemodynamic (i.e. blood pressure) sequelae following central CRF application and thus indicates that this mechanism is of physiological significance for learned stress responses.</abstract><qualityIndicators><score>4.688</score><pdfVersion>1.4</pdfVersion><pdfPageSize>504 x 719.759 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>986</abstractCharCount><pdfWordCount>2616</pdfWordCount><pdfCharCount>16395</pdfCharCount><pdfPageCount>5</pdfPageCount><abstractWordCount>131</abstractWordCount></qualityIndicators><title>Pavlovian conditioning of corticotropin‐releasing factor‐induced increase of blood pressure and corticosterone secretion in the rat</title><refBibs><json:item><author><json:item><name>J. 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research</json:string><json:string>physiology</json:string></scienceMetrix></categories><publicationDate>1992</publicationDate><copyrightDate>1992</copyrightDate><doi><json:string>10.1111/j.1748-1716.1992.tb09336.x</json:string></doi><id>953AA63343A9B048E07CE68CE9682C9F163A19F4</id><score>0.722759</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/953AA63343A9B048E07CE68CE9682C9F163A19F4/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/953AA63343A9B048E07CE68CE9682C9F163A19F4/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/953AA63343A9B048E07CE68CE9682C9F163A19F4/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Pavlovian conditioning of corticotropin‐releasing factor‐induced increase of blood pressure and corticosterone secretion in the rat</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>© 1992 Scandinavian Physiological Society</p></availability><date>1992</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Pavlovian conditioning of corticotropin‐releasing factor‐induced increase of blood pressure and corticosterone secretion in the rat</title><author xml:id="author-1"><persName><forename type="first">M.</forename><surname>KREUTZ</surname></persName><affiliation>Department of Molecular Neuroendocrinology, Max‐Planck‐Institute of Experimental Medicine, Göttingen, FRG</affiliation></author><author xml:id="author-2"><persName><forename type="first">D.</forename><surname>HELLHAMMER</surname></persName><affiliation>Department of Physiological and Clinical Psychology, University of Trier, Trier‐Tarforst, Germany</affiliation></author><author xml:id="author-3"><persName><forename type="first">R.</forename><surname>MURISON</surname></persName><affiliation>Department of Physiological Psychology, University of Bergen, Bergen, Norway</affiliation></author><author xml:id="author-4"><persName><forename type="first">H.</forename><surname>VETTER</surname></persName><affiliation>Department of Internal Medicine (Medizinische Poliklinik), Bonn, Germany</affiliation></author><author xml:id="author-5"><persName><forename type="first">U.</forename><surname>KRAUSE</surname></persName><affiliation>Department of Internal Medicine‐ Endocrinology and Metabolism, University of Mainz, Mainz, Germany</affiliation></author><author xml:id="author-6"><persName><forename type="first">H.</forename><surname>LEHNERT</surname></persName><affiliation>Department of Internal Medicine‐ Endocrinology and Metabolism, University of Mainz, Mainz, Germany</affiliation><affiliation>Department of Internal Medicine (Endocrinology and Metabolism), University of Mainz, Langenbeckstrasse 1, 6500 Mainz, Germany.</affiliation></author></analytic><monogr><title level="j">Acta Physiologica Scandinavica</title><idno type="pISSN">0001-6772</idno><idno type="eISSN">1365-201X</idno><idno type="DOI">10.1111/(ISSN)1365-201X</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1992-05"></date><biblScope unit="volume">145</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="59">59</biblScope><biblScope unit="page" to="63">63</biblScope></imprint></monogr><idno type="istex">953AA63343A9B048E07CE68CE9682C9F163A19F4</idno><idno type="DOI">10.1111/j.1748-1716.1992.tb09336.x</idno><idno type="ArticleID">APHA59</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1992</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Corticotropin‐releasing factor (CRF) is clearly involved in the central regulation of the pituitary‐adrenal axis and, moreover, of autonomic nervous system functions. Enhanced sympathetic activity with subsequent increases in blood pressure and heart rate and attenuation of the baroreceptor reflex results from the intracerebroventricular (i.c.v.) administration of CRF. Additionally, the peptide has a variety of potent effects on behavioural responses in animals similar to those observed after an experimentally evoked stress. It was therefore of obvious interest to examine whether CRF is a possible mediator of the learning processes associated with physiological stress reaction patterns. This report clearly demonstrates a classical conditioning of the endocrine (i.e. corticosterone secretion) and haemodynamic (i.e. blood pressure) sequelae following central CRF application and thus indicates that this mechanism is of physiological significance for learned stress responses.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>keywords</head><item><term>blood pressure</term></item><item><term>classical conditioning</term></item><item><term>corticosterone</term></item><item><term>corticotropinreleasing factor.</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1992-05">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/953AA63343A9B048E07CE68CE9682C9F163A19F4/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: 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Enhanced sympathetic activity with subsequent increases in blood pressure and heart rate and attenuation of the baroreceptor reflex results from the intracerebroventricular (i.c.v.) administration of CRF. Additionally, the peptide has a variety of potent effects on behavioural responses in animals similar to those observed after an experimentally evoked stress. It was therefore of obvious interest to examine whether CRF is a possible mediator of the learning processes associated with physiological stress reaction patterns. This report clearly demonstrates a classical conditioning of the endocrine (i.e. corticosterone secretion) and haemodynamic (i.e. blood pressure) sequelae following central CRF application and thus indicates that this mechanism is of physiological significance for learned stress responses.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Pavlovian conditioning of corticotropin‐releasing factor‐induced increase of blood pressure and corticosterone secretion in the rat</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Pavlovian conditioning of corticotropin‐releasing factor‐induced increase of blood pressure and corticosterone secretion in the rat</title></titleInfo><name type="personal"><namePart type="given">M.</namePart><namePart type="family">KREUTZ</namePart><affiliation>Department of Molecular Neuroendocrinology, Max‐Planck‐Institute of Experimental Medicine, Göttingen, FRG</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D.</namePart><namePart type="family">HELLHAMMER</namePart><affiliation>Department of Physiological and Clinical Psychology, University of Trier, Trier‐Tarforst, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R.</namePart><namePart type="family">MURISON</namePart><affiliation>Department of Physiological Psychology, University of Bergen, Bergen, Norway</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H.</namePart><namePart type="family">VETTER</namePart><affiliation>Department of Internal Medicine (Medizinische Poliklinik), Bonn, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">U.</namePart><namePart type="family">KRAUSE</namePart><affiliation>Department of Internal Medicine‐ Endocrinology and Metabolism, University of Mainz, Mainz, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H.</namePart><namePart type="family">LEHNERT</namePart><affiliation>Department of Internal Medicine‐ Endocrinology and Metabolism, University of Mainz, Mainz, Germany</affiliation><affiliation>Department of Internal Medicine (Endocrinology and Metabolism), University of Mainz, Langenbeckstrasse 1, 6500 Mainz, Germany.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">1992-05</dateIssued><edition>Received 27 June 1991, accepted 8 January 1992</edition><copyrightDate encoding="w3cdtf">1992</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="references">24</extent></physicalDescription><abstract lang="en">Corticotropin‐releasing factor (CRF) is clearly involved in the central regulation of the pituitary‐adrenal axis and, moreover, of autonomic nervous system functions. Enhanced sympathetic activity with subsequent increases in blood pressure and heart rate and attenuation of the baroreceptor reflex results from the intracerebroventricular (i.c.v.) administration of CRF. Additionally, the peptide has a variety of potent effects on behavioural responses in animals similar to those observed after an experimentally evoked stress. It was therefore of obvious interest to examine whether CRF is a possible mediator of the learning processes associated with physiological stress reaction patterns. This report clearly demonstrates a classical conditioning of the endocrine (i.e. corticosterone secretion) and haemodynamic (i.e. blood pressure) sequelae following central CRF application and thus indicates that this mechanism is of physiological significance for learned stress responses.</abstract><subject lang="en"><genre>keywords</genre><topic>blood pressure</topic><topic>classical conditioning</topic><topic>corticosterone</topic><topic>corticotropinreleasing factor.</topic></subject><relatedItem type="host"><titleInfo><title>Acta Physiologica Scandinavica</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0001-6772</identifier><identifier type="eISSN">1365-201X</identifier><identifier type="DOI">10.1111/(ISSN)1365-201X</identifier><identifier type="PublisherID">APHA</identifier><part><date>1992</date><detail type="volume"><caption>vol.</caption><number>145</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>59</start><end>63</end><total>5</total></extent></part></relatedItem><identifier type="istex">953AA63343A9B048E07CE68CE9682C9F163A19F4</identifier><identifier type="DOI">10.1111/j.1748-1716.1992.tb09336.x</identifier><identifier type="ArticleID">APHA59</identifier><accessCondition type="use and reproduction" contentType="copyright">© 1992 Scandinavian Physiological Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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