Evidence that corticotropin-releasing factor within the extended amygdala mediates the activation of tryptophan hydroxylase produced by sound stress in the rat
Identifieur interne : 001416 ( Istex/Corpus ); précédent : 001415; suivant : 001417Evidence that corticotropin-releasing factor within the extended amygdala mediates the activation of tryptophan hydroxylase produced by sound stress in the rat
Auteurs : Margaret C. Boadle-Biber ; Virendra B. Singh ; Karl C. Corley ; Tam-Hao Phan ; Roger P. DiltsSource :
- Brain Research [ 0006-8993 ] ; 1993.
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Abstract
Abstract: Non-endocrine corticotropin-releasing factor (CRF) is believed to be involved in mediating stress behaviors in rats. The present study investigated the role of CRF in mediating the activation of tryptophan hydroxylase, the rate-limiting enzyme in serotonin synthesis, produced in response to sound stress. Bilateral injections of 0.5–3.0 μg of CRF directed towards the central nucleus of the amygdala increased tryptophan hydroxylase activity measured ex vivo when compared to vehicle-injected controls. This increase in enzyme activity, like that due to sound stress, was reversed in vitro by alkaline phosphatase. Intra-amygdala CRF (0.5 μg) also enhanced the in vivo accumulation of 5-hydroxytryptophan (5-HTP) following the administration ofm-hydroxylbenzylamine (NSD-1015, 200 mg/kg). The activation of tryptophan hydroxylase, produced by intra-amygdala CRF, was blocked by the CRF receptor antagonist α-helical CRF9–41 (10 μg). Additionally, the 5-HT1A agonist, gepirone, given either systemically (10 mg/kg) or intracerebrally into the region of the dorsal raphe (14 μg), blocked the tryptophan hydroxylase response to CRF. CRF did not increase tissue levels of 5-hydroxyindole acetic acid (5-HIAA) or the ratio of 5-HIAA to serotonin (5-HT) within the striatum of the same animals in which tryptophan hydroxylase activity was quantified, an effect produced by sound stress. Thus, while intra-amygdala CRF failed to mimic the sound stress response in its entirety, these data suggest that CRF is involved in mediating the activation of tryptophan hydroxylase produced by sound stress within the midbrain serotonin neurons.
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DOI: 10.1016/0006-8993(93)90944-I
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Evidence that corticotropin-releasing factor within the extended amygdala mediates the activation of tryptophan hydroxylase produced by sound stress in the rat</title><author><name sortKey="Boadle Biber, Margaret C" sort="Boadle Biber, Margaret C" uniqKey="Boadle Biber M" first="Margaret C." last="Boadle-Biber">Margaret C. Boadle-Biber</name><affiliation><mods:affiliation>Department of Physiology, PO Box 551, M.C.V. Station, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0551, USA</mods:affiliation></affiliation></author><author><name sortKey="Singh, Virendra B" sort="Singh, Virendra B" uniqKey="Singh V" first="Virendra B." last="Singh">Virendra B. Singh</name><affiliation><mods:affiliation>Department of Physiology, PO Box 551, M.C.V. Station, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0551, USA</mods:affiliation></affiliation></author><author><name sortKey="Corley, Karl C" sort="Corley, Karl C" uniqKey="Corley K" first="Karl C." last="Corley">Karl C. Corley</name><affiliation><mods:affiliation>Department of Physiology, PO Box 551, M.C.V. Station, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0551, USA</mods:affiliation></affiliation></author><author><name sortKey="Phan, Tam Hao" sort="Phan, Tam Hao" uniqKey="Phan T" first="Tam-Hao" last="Phan">Tam-Hao Phan</name><affiliation><mods:affiliation>Department of Physiology, PO Box 551, M.C.V. Station, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0551, USA</mods:affiliation></affiliation></author><author><name sortKey="Dilts, Roger P" sort="Dilts, Roger P" uniqKey="Dilts R" first="Roger P." last="Dilts">Roger P. Dilts</name><affiliation><mods:affiliation>Department of Physiology, PO Box 551, M.C.V. 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Boadle-Biber</name><affiliation><mods:affiliation>Department of Physiology, PO Box 551, M.C.V. Station, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0551, USA</mods:affiliation></affiliation></author><author><name sortKey="Singh, Virendra B" sort="Singh, Virendra B" uniqKey="Singh V" first="Virendra B." last="Singh">Virendra B. Singh</name><affiliation><mods:affiliation>Department of Physiology, PO Box 551, M.C.V. Station, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0551, USA</mods:affiliation></affiliation></author><author><name sortKey="Corley, Karl C" sort="Corley, Karl C" uniqKey="Corley K" first="Karl C." last="Corley">Karl C. Corley</name><affiliation><mods:affiliation>Department of Physiology, PO Box 551, M.C.V. Station, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0551, USA</mods:affiliation></affiliation></author><author><name sortKey="Phan, Tam Hao" sort="Phan, Tam Hao" uniqKey="Phan T" first="Tam-Hao" last="Phan">Tam-Hao Phan</name><affiliation><mods:affiliation>Department of Physiology, PO Box 551, M.C.V. Station, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0551, USA</mods:affiliation></affiliation></author><author><name sortKey="Dilts, Roger P" sort="Dilts, Roger P" uniqKey="Dilts R" first="Roger P." last="Dilts">Roger P. Dilts</name><affiliation><mods:affiliation>Department of Physiology, PO Box 551, M.C.V. Station, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0551, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Brain Research</title><title level="j" type="abbrev">BRES</title><idno type="ISSN">0006-8993</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1993">1993</date><biblScope unit="volume">628</biblScope><biblScope unit="issue">1–2</biblScope><biblScope unit="page" from="105">105</biblScope><biblScope unit="page" to="114">114</biblScope></imprint><idno type="ISSN">0006-8993</idno></series><idno type="istex">5F5FD680BE20824909F85DCEA6C54F5C68CA06E5</idno><idno type="DOI">10.1016/0006-8993(93)90944-I</idno><idno type="PII">0006-8993(93)90944-I</idno><idno type="ArticleID">9390944I</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-8993</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>5-Hydroxytryptophan</term><term>5-hydroxyindole acetic acid (5-HIAA)</term><term>CRH</term><term>Central nucleus</term><term>Corticotropin-releasing factor</term><term>Dorsal raphe</term><term>Gepirone</term><term>Metabolism</term><term>Noise</term><term>Serotonin (5-HT)</term><term>Serotonin 5-HT1A receptor</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Non-endocrine corticotropin-releasing factor (CRF) is believed to be involved in mediating stress behaviors in rats. The present study investigated the role of CRF in mediating the activation of tryptophan hydroxylase, the rate-limiting enzyme in serotonin synthesis, produced in response to sound stress. Bilateral injections of 0.5–3.0 μg of CRF directed towards the central nucleus of the amygdala increased tryptophan hydroxylase activity measured ex vivo when compared to vehicle-injected controls. This increase in enzyme activity, like that due to sound stress, was reversed in vitro by alkaline phosphatase. Intra-amygdala CRF (0.5 μg) also enhanced the in vivo accumulation of 5-hydroxytryptophan (5-HTP) following the administration ofm-hydroxylbenzylamine (NSD-1015, 200 mg/kg). The activation of tryptophan hydroxylase, produced by intra-amygdala CRF, was blocked by the CRF receptor antagonist α-helical CRF9–41 (10 μg). Additionally, the 5-HT1A agonist, gepirone, given either systemically (10 mg/kg) or intracerebrally into the region of the dorsal raphe (14 μg), blocked the tryptophan hydroxylase response to CRF. CRF did not increase tissue levels of 5-hydroxyindole acetic acid (5-HIAA) or the ratio of 5-HIAA to serotonin (5-HT) within the striatum of the same animals in which tryptophan hydroxylase activity was quantified, an effect produced by sound stress. Thus, while intra-amygdala CRF failed to mimic the sound stress response in its entirety, these data suggest that CRF is involved in mediating the activation of tryptophan hydroxylase produced by sound stress within the midbrain serotonin neurons.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Margaret C. Boadle-Biber</name><affiliations><json:string>Department of Physiology, PO Box 551, M.C.V. Station, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0551, USA</json:string></affiliations></json:item><json:item><name>Virendra B. Singh</name><affiliations><json:string>Department of Physiology, PO Box 551, M.C.V. Station, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0551, USA</json:string></affiliations></json:item><json:item><name>Karl C. Corley</name><affiliations><json:string>Department of Physiology, PO Box 551, M.C.V. Station, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0551, USA</json:string></affiliations></json:item><json:item><name>Tam-Hao Phan</name><affiliations><json:string>Department of Physiology, PO Box 551, M.C.V. Station, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0551, USA</json:string></affiliations></json:item><json:item><name>Roger P. Dilts</name><affiliations><json:string>Department of Physiology, PO Box 551, M.C.V. Station, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0551, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>5-Hydroxytryptophan</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Serotonin (5-HT)</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>5-hydroxyindole acetic acid (5-HIAA)</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Central nucleus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Dorsal raphe</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Corticotropin-releasing factor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>CRH</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Metabolism</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Gepirone</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Serotonin 5-HT1A receptor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Noise</value></json:item></subject><articleId><json:string>9390944I</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>Short communication</json:string></originalGenre><abstract>Non-endocrine corticotropin-releasing factor (CRF) is believed to be involved in mediating stress behaviors in rats. The present study investigated the role of CRF in mediating the activation of tryptophan hydroxylase, the rate-limiting enzyme in serotonin synthesis, produced in response to sound stress. Bilateral injections of 0.5–3.0 μg of CRF directed towards the central nucleus of the amygdala increased tryptophan hydroxylase activity measured ex vivo when compared to vehicle-injected controls. This increase in enzyme activity, like that due to sound stress, was reversed in vitro by alkaline phosphatase. Intra-amygdala CRF (0.5 μg) also enhanced the in vivo accumulation of 5-hydroxytryptophan (5-HTP) following the administration ofm-hydroxylbenzylamine (NSD-1015, 200 mg/kg). The activation of tryptophan hydroxylase, produced by intra-amygdala CRF, was blocked by the CRF receptor antagonist α-helical CRF9–41 (10 μg). Additionally, the 5-HT1A agonist, gepirone, given either systemically (10 mg/kg) or intracerebrally into the region of the dorsal raphe (14 μg), blocked the tryptophan hydroxylase response to CRF. CRF did not increase tissue levels of 5-hydroxyindole acetic acid (5-HIAA) or the ratio of 5-HIAA to serotonin (5-HT) within the striatum of the same animals in which tryptophan hydroxylase activity was quantified, an effect produced by sound stress. Thus, while intra-amygdala CRF failed to mimic the sound stress response in its entirety, these data suggest that CRF is involved in mediating the activation of tryptophan hydroxylase produced by sound stress within the midbrain serotonin neurons.</abstract><qualityIndicators><score>7.772</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 814 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>11</keywordCount><abstractCharCount>1629</abstractCharCount><pdfWordCount>7387</pdfWordCount><pdfCharCount>41302</pdfCharCount><pdfPageCount>10</pdfPageCount><abstractWordCount>231</abstractWordCount></qualityIndicators><title>Evidence that corticotropin-releasing factor within the extended amygdala mediates the activation of tryptophan hydroxylase produced by sound stress in the rat</title><pii><json:string>0006-8993(93)90944-I</json:string></pii><genre><json:string>brief-communication</json:string></genre><serie><pages><last>334</last><first>223</first></pages><language><json:string>unknown</json:string></language><title>The Rat Nervous System,Vol. 1, Forebrain and Midbrain</title></serie><host><volume>628</volume><pii><json:string>S0006-8993(00)X0654-3</json:string></pii><pages><last>114</last><first>105</first></pages><issn><json:string>0006-8993</json:string></issn><issue>1–2</issue><genre><json:string>journal</json:string></genre><language><json:string>unknown</json:string></language><title>Brain Research</title><publicationDate>1993</publicationDate></host><categories><wos><json:string>NEUROSCIENCES</json:string></wos></categories><publicationDate>1993</publicationDate><copyrightDate>1993</copyrightDate><doi><json:string>10.1016/0006-8993(93)90944-I</json:string></doi><id>5F5FD680BE20824909F85DCEA6C54F5C68CA06E5</id><score>0.04088016</score><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/5F5FD680BE20824909F85DCEA6C54F5C68CA06E5/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/5F5FD680BE20824909F85DCEA6C54F5C68CA06E5/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/5F5FD680BE20824909F85DCEA6C54F5C68CA06E5/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Evidence that corticotropin-releasing factor within the extended amygdala mediates the activation of tryptophan hydroxylase produced by sound stress in the rat</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>ELSEVIER</publisher><availability><p>©1993 Elsevier Science Publishers B.V. All rights reserved</p></availability><date>1993</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Evidence that corticotropin-releasing factor within the extended amygdala mediates the activation of tryptophan hydroxylase produced by sound stress in the rat</title><author xml:id="author-1"><persName><forename type="first">Margaret C.</forename><surname>Boadle-Biber</surname></persName><note type="correspondence"><p>Corresponding author. Fax: (1) (804) 371-7382.</p></note><affiliation>Department of Physiology, PO Box 551, M.C.V. Station, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0551, USA</affiliation></author><author xml:id="author-2"><persName><forename type="first">Virendra B.</forename><surname>Singh</surname></persName><affiliation>Department of Physiology, PO Box 551, M.C.V. Station, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0551, USA</affiliation></author><author xml:id="author-3"><persName><forename type="first">Karl C.</forename><surname>Corley</surname></persName><affiliation>Department of Physiology, PO Box 551, M.C.V. Station, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0551, USA</affiliation></author><author xml:id="author-4"><persName><forename type="first">Tam-Hao</forename><surname>Phan</surname></persName><affiliation>Department of Physiology, PO Box 551, M.C.V. Station, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0551, USA</affiliation></author><author xml:id="author-5"><persName><forename type="first">Roger P.</forename><surname>Dilts</surname></persName><affiliation>Department of Physiology, PO Box 551, M.C.V. Station, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0551, USA</affiliation></author></analytic><monogr><title level="j">Brain Research</title><title level="j" type="abbrev">BRES</title><idno type="pISSN">0006-8993</idno><idno type="PII">S0006-8993(00)X0654-3</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1993"></date><biblScope unit="volume">628</biblScope><biblScope unit="issue">1–2</biblScope><biblScope unit="page" from="105">105</biblScope><biblScope unit="page" to="114">114</biblScope></imprint></monogr><idno type="istex">5F5FD680BE20824909F85DCEA6C54F5C68CA06E5</idno><idno type="DOI">10.1016/0006-8993(93)90944-I</idno><idno type="PII">0006-8993(93)90944-I</idno><idno type="ArticleID">9390944I</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1993</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: Non-endocrine corticotropin-releasing factor (CRF) is believed to be involved in mediating stress behaviors in rats. The present study investigated the role of CRF in mediating the activation of tryptophan hydroxylase, the rate-limiting enzyme in serotonin synthesis, produced in response to sound stress. Bilateral injections of 0.5–3.0 μg of CRF directed towards the central nucleus of the amygdala increased tryptophan hydroxylase activity measured ex vivo when compared to vehicle-injected controls. This increase in enzyme activity, like that due to sound stress, was reversed in vitro by alkaline phosphatase. Intra-amygdala CRF (0.5 μg) also enhanced the in vivo accumulation of 5-hydroxytryptophan (5-HTP) following the administration ofm-hydroxylbenzylamine (NSD-1015, 200 mg/kg). The activation of tryptophan hydroxylase, produced by intra-amygdala CRF, was blocked by the CRF receptor antagonist α-helical CRF9–41 (10 μg). Additionally, the 5-HT1A agonist, gepirone, given either systemically (10 mg/kg) or intracerebrally into the region of the dorsal raphe (14 μg), blocked the tryptophan hydroxylase response to CRF. CRF did not increase tissue levels of 5-hydroxyindole acetic acid (5-HIAA) or the ratio of 5-HIAA to serotonin (5-HT) within the striatum of the same animals in which tryptophan hydroxylase activity was quantified, an effect produced by sound stress. Thus, while intra-amygdala CRF failed to mimic the sound stress response in its entirety, these data suggest that CRF is involved in mediating the activation of tryptophan hydroxylase produced by sound stress within the midbrain serotonin neurons.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>5-Hydroxytryptophan</term></item><item><term>Serotonin (5-HT)</term></item><item><term>5-hydroxyindole acetic acid (5-HIAA)</term></item><item><term>Central nucleus</term></item><item><term>Dorsal raphe</term></item><item><term>Corticotropin-releasing factor</term></item><item><term>CRH</term></item><item><term>Metabolism</term></item><item><term>Gepirone</term></item><item><term>Serotonin 5-HT1A receptor</term></item><item><term>Noise</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1993">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/5F5FD680BE20824909F85DCEA6C54F5C68CA06E5/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier doc found" wicri:toSee="Elsevier, no converted or simple article"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 5.0.1//EN//XML" URI="art501.dtd" name="istex:docType"></istex:docType><istex:document><article version="5.0" xml:lang="en" docsubtype="sco"><item-info><jid>BRES</jid><aid>9390944I</aid><ce:pii>0006-8993(93)90944-I</ce:pii><ce:doi>10.1016/0006-8993(93)90944-I</ce:doi><ce:copyright type="unknown" year="1993">Elsevier Science Publishers B.V. All rights reserved</ce:copyright></item-info><head><ce:title>Evidence that corticotropin-releasing factor within the extended amygdala mediates the activation of tryptophan hydroxylase produced by sound stress in the rat</ce:title><ce:author-group><ce:author><ce:given-name>Margaret C.</ce:given-name><ce:surname>Boadle-Biber</ce:surname><ce:cross-ref refid="cor1"><ce:sup loc="post">*</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Virendra B.</ce:given-name><ce:surname>Singh</ce:surname></ce:author><ce:author><ce:given-name>Karl C.</ce:given-name><ce:surname>Corley</ce:surname></ce:author><ce:author><ce:given-name>Tam-Hao</ce:given-name><ce:surname>Phan</ce:surname></ce:author><ce:author><ce:given-name>Roger P.</ce:given-name><ce:surname>Dilts</ce:surname></ce:author><ce:affiliation><ce:textfn>Department of Physiology, PO Box 551, M.C.V. Station, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0551, USA</ce:textfn></ce:affiliation><ce:correspondence id="cor1"><ce:label>*</ce:label><ce:text>Corresponding author. Fax: (1) (804) 371-7382.</ce:text></ce:correspondence></ce:author-group><ce:date-accepted day="22" month="6" year="1993"></ce:date-accepted><ce:abstract id="ab1" class="author" xml:lang="en"><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para view="all" id="simple-para.0010">Non-endocrine corticotropin-releasing factor (CRF) is believed to be involved in mediating stress behaviors in rats. The present study investigated the role of CRF in mediating the activation of tryptophan hydroxylase, the rate-limiting enzyme in serotonin synthesis, produced in response to sound stress. Bilateral injections of 0.5–3.0 μg of CRF directed towards the central nucleus of the amygdala increased tryptophan hydroxylase activity measured ex vivo when compared to vehicle-injected controls. This increase in enzyme activity, like that due to sound stress, was reversed in vitro by alkaline phosphatase. Intra-amygdala CRF (0.5 μg) also enhanced the in vivo accumulation of 5-hydroxytryptophan (5-HTP) following the administration of<ce:italic>m</ce:italic>-hydroxylbenzylamine (NSD-1015, 200 mg/kg). The activation of tryptophan hydroxylase, produced by intra-amygdala CRF, was blocked by the CRF receptor antagonist α-helical CRF<ce:inf loc="post">9–41</ce:inf> (10 μg). Additionally, the 5-HT<ce:inf loc="post">1A</ce:inf> agonist, gepirone, given either systemically (10 mg/kg) or intracerebrally into the region of the dorsal raphe (14 μg), blocked the tryptophan hydroxylase response to CRF. CRF did not increase tissue levels of 5-hydroxyindole acetic acid (5-HIAA) or the ratio of 5-HIAA to serotonin (5-HT) within the striatum of the same animals in which tryptophan hydroxylase activity was quantified, an effect produced by sound stress. Thus, while intra-amygdala CRF failed to mimic the sound stress response in its entirety, these data suggest that CRF is involved in mediating the activation of tryptophan hydroxylase produced by sound stress within the midbrain serotonin neurons.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords class="keyword" xml:lang="en"><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>5-Hydroxytryptophan</ce:text></ce:keyword><ce:keyword><ce:text>Serotonin (5-HT)</ce:text></ce:keyword><ce:keyword><ce:text>5-hydroxyindole acetic acid (5-HIAA)</ce:text></ce:keyword><ce:keyword><ce:text>Central nucleus</ce:text></ce:keyword><ce:keyword><ce:text>Dorsal raphe</ce:text></ce:keyword><ce:keyword><ce:text>Corticotropin-releasing factor</ce:text></ce:keyword><ce:keyword><ce:text>CRH</ce:text></ce:keyword><ce:keyword><ce:text>Metabolism</ce:text></ce:keyword><ce:keyword><ce:text>Gepirone</ce:text></ce:keyword><ce:keyword><ce:text>Serotonin 5-HT<ce:inf loc="post">1A</ce:inf> receptor</ce:text></ce:keyword><ce:keyword><ce:text>Noise</ce:text></ce:keyword></ce:keywords></head><tail view="all"><ce:bibliography view="all" id="bibliography.0010"><ce:section-title>Reference</ce:section-title><ce:bibliography-sec id="bibliography-sec.0010"><ce:bib-reference id="bib1"><ce:label>1</ce:label><sb:reference><sb:contribution langtype="en"><sb:authors><sb:author><ce:surname>Alheid</ce:surname><ce:given-name>G.F.</ce:given-name></sb:author><sb:author><ce:surname>Heimer</ce:surname><ce:given-name>L.</ce:given-name></sb:author></sb:authors><sb:title><sb:maintitle>New perspectives in basal forebrain organization of special relevance for neuropsychiatric disorders; the striatopallidal, amygdaloid, and corticopetal components of substantia innominata</sb:maintitle></sb:title></sb:contribution><sb:host><sb:issue><sb:series><sb:title><sb:maintitle>Neuroscience</sb:maintitle></sb:title><sb:volume-nr>27</sb:volume-nr></sb:series><sb:date>1988</sb:date></sb:issue><sb:pages><sb:first-page>1</sb:first-page><sb:last-page>39</sb:last-page></sb:pages></sb:host></sb:reference></ce:bib-reference><ce:bib-reference id="bib2"><ce:label>2</ce:label><sb:reference><sb:contribution langtype="en"><sb:authors><sb:author><ce:surname>Bianchi</ce:surname><ce:given-name>G.</ce:given-name></sb:author><sb:author><ce:surname>Caccia</ce:surname><ce:given-name>S.</ce:given-name></sb:author><sb:author><ce:surname>Vedova</ce:surname><ce:given-name>C.F.</ce:given-name></sb:author><sb:author><ce:surname>Garattini</ce:surname><ce:given-name>S.</ce:given-name></sb:author></sb:authors><sb:title><sb:maintitle>The alpha-2-adrenoreceptor antagonist activity of ipsapirone and gepirone is mediated by their common metabolite 1-(2-pyrimidinyl)-piperazine (PmP)</sb:maintitle></sb:title></sb:contribution><sb:host><sb:issue><sb:series><sb:title><sb:maintitle>Eur. 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Neurochem.</sb:maintitle></sb:title><sb:volume-nr>46</sb:volume-nr></sb:series><sb:date>1986</sb:date></sb:issue><sb:pages><sb:first-page>61</sb:first-page><sb:last-page>67</sb:last-page></sb:pages></sb:host></sb:reference></ce:bib-reference></ce:bibliography-sec></ce:bibliography></tail></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Evidence that corticotropin-releasing factor within the extended amygdala mediates the activation of tryptophan hydroxylase produced by sound stress in the rat</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Evidence that corticotropin-releasing factor within the extended amygdala mediates the activation of tryptophan hydroxylase produced by sound stress in the rat</title></titleInfo><name type="personal"><namePart type="given">Margaret C.</namePart><namePart type="family">Boadle-Biber</namePart><affiliation>Department of Physiology, PO Box 551, M.C.V. Station, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0551, USA</affiliation><description>Corresponding author. Fax: (1) (804) 371-7382.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Virendra B.</namePart><namePart type="family">Singh</namePart><affiliation>Department of Physiology, PO Box 551, M.C.V. Station, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0551, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Karl C.</namePart><namePart type="family">Corley</namePart><affiliation>Department of Physiology, PO Box 551, M.C.V. Station, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0551, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tam-Hao</namePart><namePart type="family">Phan</namePart><affiliation>Department of Physiology, PO Box 551, M.C.V. Station, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0551, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Roger P.</namePart><namePart type="family">Dilts</namePart><affiliation>Department of Physiology, PO Box 551, M.C.V. Station, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0551, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="brief-communication" displayLabel="Short communication"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1993</dateIssued><copyrightDate encoding="w3cdtf">1993</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Abstract: Non-endocrine corticotropin-releasing factor (CRF) is believed to be involved in mediating stress behaviors in rats. The present study investigated the role of CRF in mediating the activation of tryptophan hydroxylase, the rate-limiting enzyme in serotonin synthesis, produced in response to sound stress. Bilateral injections of 0.5–3.0 μg of CRF directed towards the central nucleus of the amygdala increased tryptophan hydroxylase activity measured ex vivo when compared to vehicle-injected controls. This increase in enzyme activity, like that due to sound stress, was reversed in vitro by alkaline phosphatase. Intra-amygdala CRF (0.5 μg) also enhanced the in vivo accumulation of 5-hydroxytryptophan (5-HTP) following the administration ofm-hydroxylbenzylamine (NSD-1015, 200 mg/kg). The activation of tryptophan hydroxylase, produced by intra-amygdala CRF, was blocked by the CRF receptor antagonist α-helical CRF9–41 (10 μg). Additionally, the 5-HT1A agonist, gepirone, given either systemically (10 mg/kg) or intracerebrally into the region of the dorsal raphe (14 μg), blocked the tryptophan hydroxylase response to CRF. CRF did not increase tissue levels of 5-hydroxyindole acetic acid (5-HIAA) or the ratio of 5-HIAA to serotonin (5-HT) within the striatum of the same animals in which tryptophan hydroxylase activity was quantified, an effect produced by sound stress. Thus, while intra-amygdala CRF failed to mimic the sound stress response in its entirety, these data suggest that CRF is involved in mediating the activation of tryptophan hydroxylase produced by sound stress within the midbrain serotonin neurons.</abstract><subject lang="en"><genre>Keywords</genre><topic>5-Hydroxytryptophan</topic><topic>Serotonin (5-HT)</topic><topic>5-hydroxyindole acetic acid (5-HIAA)</topic><topic>Central nucleus</topic><topic>Dorsal raphe</topic><topic>Corticotropin-releasing factor</topic><topic>CRH</topic><topic>Metabolism</topic><topic>Gepirone</topic><topic>Serotonin 5-HT1A receptor</topic><topic>Noise</topic></subject><relatedItem type="host"><titleInfo><title>Brain Research</title></titleInfo><titleInfo type="abbreviated"><title>BRES</title></titleInfo><genre type="journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">19931119</dateIssued></originInfo><identifier type="ISSN">0006-8993</identifier><identifier type="PII">S0006-8993(00)X0654-3</identifier><part><date>19931119</date><detail type="volume"><number>628</number><caption>vol.</caption></detail><detail type="issue"><number>1–2</number><caption>no.</caption></detail><extent unit="issue pages"><start>1</start><end>360</end></extent><extent unit="pages"><start>105</start><end>114</end></extent></part></relatedItem><identifier type="istex">5F5FD680BE20824909F85DCEA6C54F5C68CA06E5</identifier><identifier type="DOI">10.1016/0006-8993(93)90944-I</identifier><identifier type="PII">0006-8993(93)90944-I</identifier><identifier type="ArticleID">9390944I</identifier><accessCondition type="use and reproduction" contentType="copyright">©1993 Elsevier Science Publishers B.V. 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