Loading…
Chronic citalopram treatment does not sensitize the adrenal gland to ACTH (1—24) in rats
We have previously reported that rats exposed chronically to citalopram are able to elicit a corticosterone but not adrenocorticotropic hormone (ACTH) response to restraint stress. Thus we proposed the hypothesis that the corticosterone response to restraint in citalopram-treated rats was maintained...
Saved in:
| Published in: | Journal of psychopharmacology (Oxford) 2007-11, Vol.21 (8), p.885-887 |
|---|---|
| Main Authors: | , , |
| Format: | Article |
| Language: | English |
| Subjects: | |
| Citations: | Items that this one cites Items that cite this one |
| Online Access: | Get full text |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| cited_by | cdi_FETCH-LOGICAL-c464t-ab4227ce146ebc762b74b96da20cb0bc2adc8ed552c2872e29d968f06f97966c3 |
|---|---|
| cites | cdi_FETCH-LOGICAL-c464t-ab4227ce146ebc762b74b96da20cb0bc2adc8ed552c2872e29d968f06f97966c3 |
| container_end_page | 887 |
| container_issue | 8 |
| container_start_page | 885 |
| container_title | Journal of psychopharmacology (Oxford) |
| container_volume | 21 |
| creator | Hesketh, S.A. Leggett, J.D. Jessop Henry, D.S. |
| description | We have previously reported that rats exposed chronically to citalopram are able to elicit a corticosterone but not adrenocorticotropic hormone (ACTH) response to restraint stress. Thus we proposed the hypothesis that the corticosterone response to restraint in citalopram-treated rats was maintained due to increased adrenal sensitivity to lower ACTH levels. To test this hypothesis, we intravenously injected ACTH (1—24) to rats (dose 3 ng/rat) exposed to citalopram through minipump infusion for 14 days and to control rats (no citalopram). ACTH significantly increased plasma corticosterone levels in both control and citalopram treated rats over a period of 120 min. There was no significant difference in plasma corticosterone between citalopram treated rats and control rats at any time point. Therefore we conclude that, under these experimental conditions, citalopram does not appear to sensitize the rodent adrenal gland to ACTH, and that other mechanisms may be responsible for the ACTH/corticosterone disconnection. |
| doi_str_mv | 10.1177/0269881107078310 |
| format | article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_746271494</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A171943631</galeid><sage_id>10.1177_0269881107078310</sage_id><sourcerecordid>A171943631</sourcerecordid><originalsourceid>FETCH-LOGICAL-c464t-ab4227ce146ebc762b74b96da20cb0bc2adc8ed552c2872e29d968f06f97966c3</originalsourceid><addsrcrecordid>eNp9kU2LFDEQhoMo7rp69yQB8evQayqdzsdxGNQVFrysFy9NOl09m6U7GZPMYT35I_yF_hIzzMDKgpJDQep5q97iJeQ5sHMApd4zLo3WAEwxpVtgD8gpCAmN4rp7SE737WbfPyFPcr5hDKSQ3WNyUrXQcdadkm_r6xSDd9T5Yue4TXahJaEtC4ZCx4iZhlhoxpB98T-QlmukdkwY7Ew3sw0jLZGu1lcX9C38_vmLi3fUB5psyU_Jo8nOGZ8d6xn5-vHD1fqiufzy6fN6ddk4IUVp7CA4Vw6rcRycknxQYjBytJy5gQ2O29FpHLuOO64VR25GI_XE5GSUkdK1Z-TNYe42xe87zKVffHY4V3MYd7lXQnIFwohKvv4vKbXQbQdtBV_eA2_iLtWTcw-Ga1CmlbJS5wdqY2fsfZhiSdbVN-LiXQw4-fq_AgV1t2yhCthB4FLMOeHUb5NfbLrtgfX7QPv7gVbJi6OT3bDgeCc4JliBV0fAZmfnKdngfL7jTCcZB1655sBlu8G_zvnX4j-Bd7Ka</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1928179366</pqid></control><display><type>article</type><title>Chronic citalopram treatment does not sensitize the adrenal gland to ACTH (1—24) in rats</title><source>Sage Journals Online</source><creator>Hesketh, S.A. ; Leggett, J.D. ; Jessop Henry, D.S.</creator><creatorcontrib>Hesketh, S.A. ; Leggett, J.D. ; Jessop Henry, D.S.</creatorcontrib><description>We have previously reported that rats exposed chronically to citalopram are able to elicit a corticosterone but not adrenocorticotropic hormone (ACTH) response to restraint stress. Thus we proposed the hypothesis that the corticosterone response to restraint in citalopram-treated rats was maintained due to increased adrenal sensitivity to lower ACTH levels. To test this hypothesis, we intravenously injected ACTH (1—24) to rats (dose 3 ng/rat) exposed to citalopram through minipump infusion for 14 days and to control rats (no citalopram). ACTH significantly increased plasma corticosterone levels in both control and citalopram treated rats over a period of 120 min. There was no significant difference in plasma corticosterone between citalopram treated rats and control rats at any time point. Therefore we conclude that, under these experimental conditions, citalopram does not appear to sensitize the rodent adrenal gland to ACTH, and that other mechanisms may be responsible for the ACTH/corticosterone disconnection.</description><identifier>ISSN: 0269-8811</identifier><identifier>EISSN: 1461-7285</identifier><identifier>DOI: 10.1177/0269881107078310</identifier><identifier>PMID: 17715205</identifier><language>eng</language><publisher>London, England: Sage Publications</publisher><subject>Adrenal gland diseases ; Adrenal glands ; Adrenal Glands - drug effects ; Adrenocorticotropic hormone ; Animals ; Antidepressants ; Biological and medical sciences ; Citalopram ; Citalopram - pharmacology ; Corticosterone ; Corticosterone - blood ; Cosyntropin - pharmacology ; Drug therapy ; Exposure ; Hypotheses ; Male ; Medical sciences ; Neuropharmacology ; Pharmacology. Drug treatments ; Physiological aspects ; Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer ; Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease) ; Psychology. Psychoanalysis. Psychiatry ; Psychopharmacology ; Rats ; Rats, Sprague-Dawley ; Rodents ; Serotonin Uptake Inhibitors - pharmacology</subject><ispartof>Journal of psychopharmacology (Oxford), 2007-11, Vol.21 (8), p.885-887</ispartof><rights>2008 INIST-CNRS</rights><rights>COPYRIGHT 2007 Sage Publications Ltd. (UK)</rights><rights>Copyright Sage Publications Ltd. Nov 2007</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c464t-ab4227ce146ebc762b74b96da20cb0bc2adc8ed552c2872e29d968f06f97966c3</citedby><cites>FETCH-LOGICAL-c464t-ab4227ce146ebc762b74b96da20cb0bc2adc8ed552c2872e29d968f06f97966c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925,79364</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19560212$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17715205$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hesketh, S.A.</creatorcontrib><creatorcontrib>Leggett, J.D.</creatorcontrib><creatorcontrib>Jessop Henry, D.S.</creatorcontrib><title>Chronic citalopram treatment does not sensitize the adrenal gland to ACTH (1—24) in rats</title><title>Journal of psychopharmacology (Oxford)</title><addtitle>J Psychopharmacol</addtitle><description>We have previously reported that rats exposed chronically to citalopram are able to elicit a corticosterone but not adrenocorticotropic hormone (ACTH) response to restraint stress. Thus we proposed the hypothesis that the corticosterone response to restraint in citalopram-treated rats was maintained due to increased adrenal sensitivity to lower ACTH levels. To test this hypothesis, we intravenously injected ACTH (1—24) to rats (dose 3 ng/rat) exposed to citalopram through minipump infusion for 14 days and to control rats (no citalopram). ACTH significantly increased plasma corticosterone levels in both control and citalopram treated rats over a period of 120 min. There was no significant difference in plasma corticosterone between citalopram treated rats and control rats at any time point. Therefore we conclude that, under these experimental conditions, citalopram does not appear to sensitize the rodent adrenal gland to ACTH, and that other mechanisms may be responsible for the ACTH/corticosterone disconnection.</description><subject>Adrenal gland diseases</subject><subject>Adrenal glands</subject><subject>Adrenal Glands - drug effects</subject><subject>Adrenocorticotropic hormone</subject><subject>Animals</subject><subject>Antidepressants</subject><subject>Biological and medical sciences</subject><subject>Citalopram</subject><subject>Citalopram - pharmacology</subject><subject>Corticosterone</subject><subject>Corticosterone - blood</subject><subject>Cosyntropin - pharmacology</subject><subject>Drug therapy</subject><subject>Exposure</subject><subject>Hypotheses</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Neuropharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Physiological aspects</subject><subject>Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer</subject><subject>Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease)</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rodents</subject><subject>Serotonin Uptake Inhibitors - pharmacology</subject><issn>0269-8811</issn><issn>1461-7285</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><recordid>eNp9kU2LFDEQhoMo7rp69yQB8evQayqdzsdxGNQVFrysFy9NOl09m6U7GZPMYT35I_yF_hIzzMDKgpJDQep5q97iJeQ5sHMApd4zLo3WAEwxpVtgD8gpCAmN4rp7SE737WbfPyFPcr5hDKSQ3WNyUrXQcdadkm_r6xSDd9T5Yue4TXahJaEtC4ZCx4iZhlhoxpB98T-QlmukdkwY7Ew3sw0jLZGu1lcX9C38_vmLi3fUB5psyU_Jo8nOGZ8d6xn5-vHD1fqiufzy6fN6ddk4IUVp7CA4Vw6rcRycknxQYjBytJy5gQ2O29FpHLuOO64VR25GI_XE5GSUkdK1Z-TNYe42xe87zKVffHY4V3MYd7lXQnIFwohKvv4vKbXQbQdtBV_eA2_iLtWTcw-Ga1CmlbJS5wdqY2fsfZhiSdbVN-LiXQw4-fq_AgV1t2yhCthB4FLMOeHUb5NfbLrtgfX7QPv7gVbJi6OT3bDgeCc4JliBV0fAZmfnKdngfL7jTCcZB1655sBlu8G_zvnX4j-Bd7Ka</recordid><startdate>20071101</startdate><enddate>20071101</enddate><creator>Hesketh, S.A.</creator><creator>Leggett, J.D.</creator><creator>Jessop Henry, D.S.</creator><general>Sage Publications</general><general>Sage</general><general>Sage Publications Ltd. (UK)</general><general>Sage Publications Ltd</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>20071101</creationdate><title>Chronic citalopram treatment does not sensitize the adrenal gland to ACTH (1—24) in rats</title><author>Hesketh, S.A. ; Leggett, J.D. ; Jessop Henry, D.S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c464t-ab4227ce146ebc762b74b96da20cb0bc2adc8ed552c2872e29d968f06f97966c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adrenal gland diseases</topic><topic>Adrenal glands</topic><topic>Adrenal Glands - drug effects</topic><topic>Adrenocorticotropic hormone</topic><topic>Animals</topic><topic>Antidepressants</topic><topic>Biological and medical sciences</topic><topic>Citalopram</topic><topic>Citalopram - pharmacology</topic><topic>Corticosterone</topic><topic>Corticosterone - blood</topic><topic>Cosyntropin - pharmacology</topic><topic>Drug therapy</topic><topic>Exposure</topic><topic>Hypotheses</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Neuropharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Physiological aspects</topic><topic>Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer</topic><topic>Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease)</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Rodents</topic><topic>Serotonin Uptake Inhibitors - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hesketh, S.A.</creatorcontrib><creatorcontrib>Leggett, J.D.</creatorcontrib><creatorcontrib>Jessop Henry, D.S.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of psychopharmacology (Oxford)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hesketh, S.A.</au><au>Leggett, J.D.</au><au>Jessop Henry, D.S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chronic citalopram treatment does not sensitize the adrenal gland to ACTH (1—24) in rats</atitle><jtitle>Journal of psychopharmacology (Oxford)</jtitle><addtitle>J Psychopharmacol</addtitle><date>2007-11-01</date><risdate>2007</risdate><volume>21</volume><issue>8</issue><spage>885</spage><epage>887</epage><pages>885-887</pages><issn>0269-8811</issn><eissn>1461-7285</eissn><abstract>We have previously reported that rats exposed chronically to citalopram are able to elicit a corticosterone but not adrenocorticotropic hormone (ACTH) response to restraint stress. Thus we proposed the hypothesis that the corticosterone response to restraint in citalopram-treated rats was maintained due to increased adrenal sensitivity to lower ACTH levels. To test this hypothesis, we intravenously injected ACTH (1—24) to rats (dose 3 ng/rat) exposed to citalopram through minipump infusion for 14 days and to control rats (no citalopram). ACTH significantly increased plasma corticosterone levels in both control and citalopram treated rats over a period of 120 min. There was no significant difference in plasma corticosterone between citalopram treated rats and control rats at any time point. Therefore we conclude that, under these experimental conditions, citalopram does not appear to sensitize the rodent adrenal gland to ACTH, and that other mechanisms may be responsible for the ACTH/corticosterone disconnection.</abstract><cop>London, England</cop><pub>Sage Publications</pub><pmid>17715205</pmid><doi>10.1177/0269881107078310</doi><tpages>3</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0269-8811 |
| ispartof | Journal of psychopharmacology (Oxford), 2007-11, Vol.21 (8), p.885-887 |
| issn | 0269-8811 1461-7285 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_746271494 |
| source | Sage Journals Online |
| subjects | Adrenal gland diseases Adrenal glands Adrenal Glands - drug effects Adrenocorticotropic hormone Animals Antidepressants Biological and medical sciences Citalopram Citalopram - pharmacology Corticosterone Corticosterone - blood Cosyntropin - pharmacology Drug therapy Exposure Hypotheses Male Medical sciences Neuropharmacology Pharmacology. Drug treatments Physiological aspects Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease) Psychology. Psychoanalysis. Psychiatry Psychopharmacology Rats Rats, Sprague-Dawley Rodents Serotonin Uptake Inhibitors - pharmacology |
| title | Chronic citalopram treatment does not sensitize the adrenal gland to ACTH (1—24) in rats |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-02T07%3A31%3A28IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Chronic%20citalopram%20treatment%20does%20not%20sensitize%20the%20adrenal%20gland%20to%20ACTH%20(1%E2%80%9424)%20in%20rats&rft.jtitle=Journal%20of%20psychopharmacology%20(Oxford)&rft.au=Hesketh,%20S.A.&rft.date=2007-11-01&rft.volume=21&rft.issue=8&rft.spage=885&rft.epage=887&rft.pages=885-887&rft.issn=0269-8811&rft.eissn=1461-7285&rft_id=info:doi/10.1177/0269881107078310&rft_dat=%3Cgale_proqu%3EA171943631%3C/gale_proqu%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c464t-ab4227ce146ebc762b74b96da20cb0bc2adc8ed552c2872e29d968f06f97966c3%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=1928179366&rft_id=info:pmid/17715205&rft_galeid=A171943631&rft_sage_id=10.1177_0269881107078310&rfr_iscdi=true |