Loading…

Glucocorticoid Fast Feedback Inhibition of Stress-Induced ACTH Secretion in the Male Rat: Rate Independence and Stress-State Resistance

Normal glucocorticoid secretion is critical for physiological and mental health. Glucocorticoid secretion is dynamically regulated by glucocorticoid-negative feedback; however, the mechanisms of that feedback process are poorly understood. We assessed the temporal characteristics of glucocorticoid-n...

Full description

Saved in:
Bibliographic Details
Published in:Endocrinology (Philadelphia) 2016-07, Vol.157 (7), p.2785-2798
Main Authors: Osterlund, Chad D, Rodriguez-Santiago, Mariana, Woodruff, Elizabeth R, Newsom, Ryan J, Chadayammuri, Anjali P, Spencer, Robert L
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-c521t-eb2cb229477a3b8020eb70e6f0f2bfcfefbec9c709894fca8796cb9c985d65873
cites cdi_FETCH-LOGICAL-c521t-eb2cb229477a3b8020eb70e6f0f2bfcfefbec9c709894fca8796cb9c985d65873
container_end_page 2798
container_issue 7
container_start_page 2785
container_title Endocrinology (Philadelphia)
container_volume 157
creator Osterlund, Chad D
Rodriguez-Santiago, Mariana
Woodruff, Elizabeth R
Newsom, Ryan J
Chadayammuri, Anjali P
Spencer, Robert L
description Normal glucocorticoid secretion is critical for physiological and mental health. Glucocorticoid secretion is dynamically regulated by glucocorticoid-negative feedback; however, the mechanisms of that feedback process are poorly understood. We assessed the temporal characteristics of glucocorticoid-negative feedback in vivo using a procedure for drug infusions and serial blood collection in unanesthetized rats that produced a minimal disruption of basal ACTH plasma levels. We compared the negative feedback effectiveness present when stress onset coincides with corticosterone's (CORT) rapidly rising phase (30 sec pretreatment), high plateau phase (15 min pretreatment), or restored basal phase (60 min pretreatment) as well as effectiveness when CORT infusion occurs after the onset of stress (5 min poststress onset). CORT treatment prior to stress onset acted remarkably fast (within 30 sec) to suppress stress-induced ACTH secretion. Furthermore, fast feedback induction did not require rapid increases in CORT at the time of stress onset (hormone rate independent), and those feedback actions were relatively long lasting (≥15 min). In contrast, CORT elevation after stress onset produced limited and delayed ACTH suppression (stress state resistance). There was a parallel stress-state resistance for CORT inhibition of stress-induced Crh heteronuclear RNA in the paraventricular nucleus but not Pomc heteronuclear RNA in the anterior pituitary. CORT treatment did not suppress stress-induced prolactin secretion, suggesting that CORT feedback is restricted to the control of hypothalamic-pituitary-adrenal axis elements of a stress response. These temporal, stress-state, and system-level features of in vivo CORT feedback provide an important physiological context for ex vivo studies of molecular and cellular mechanisms of CORT-negative feedback.
doi_str_mv 10.1210/en.2016-1123
format article
fullrecord <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4929554</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><oup_id>10.1210/en.2016-1123</oup_id><sourcerecordid>1891882829</sourcerecordid><originalsourceid>FETCH-LOGICAL-c521t-eb2cb229477a3b8020eb70e6f0f2bfcfefbec9c709894fca8796cb9c985d65873</originalsourceid><addsrcrecordid>eNqNkl1rFDEUhgdR7Fq981oCXuiFU_M1k4kXQlncdqEidOt1yGTOuKmzyZhkBH-Bf9tMd1s_UPDmhHAeHk7ynqJ4SvAJoQS_BndCMalLQii7VyyI5FUpiMD3iwXGhJWCUnFUPIrxOl855-xhcUQF4VVuLorvZ8NkvPEhWeNth1Y6JrQC6FptPqO129rWJusd8j3apAAxlmvXTQY6dLq8OkcbMAFuAOtQ2gJ6rwdAlzq9mQtkQwcj5OIMIO26W8kmzd1LiDYmnXuPiwe9HiI8OZzHxcfVu6vleXnx4Wy9PL0oTUVJKqGlpqVUciE0axtMMbQCQ93jnra96aFvwUgjsGwk741uhKxNK41sqq6uGsGOi7d77zi1O-gMuBT0oMZgdzp8U15b9XvH2a365L8qLqmsKp4FLw-C4L9MEJPa2WhgGLQDP0VFGkmahjZU_geaA6Gc31if_4Fe-ym4_BOKEYYFYTVjmXq1p0zwMQbo7-YmWM3LoMCpeRnUvAwZf_brW-_g2_Qz8GIP-Gn8l6o8qNiezFF6E6yDcY7x55R_HeAHMETNmg</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>3130713633</pqid></control><display><type>article</type><title>Glucocorticoid Fast Feedback Inhibition of Stress-Induced ACTH Secretion in the Male Rat: Rate Independence and Stress-State Resistance</title><source>Oxford University Press:Jisc Collections:OUP Read and Publish 2024-2025 (2024 collection) (Reading list)</source><creator>Osterlund, Chad D ; Rodriguez-Santiago, Mariana ; Woodruff, Elizabeth R ; Newsom, Ryan J ; Chadayammuri, Anjali P ; Spencer, Robert L</creator><creatorcontrib>Osterlund, Chad D ; Rodriguez-Santiago, Mariana ; Woodruff, Elizabeth R ; Newsom, Ryan J ; Chadayammuri, Anjali P ; Spencer, Robert L</creatorcontrib><description>Normal glucocorticoid secretion is critical for physiological and mental health. Glucocorticoid secretion is dynamically regulated by glucocorticoid-negative feedback; however, the mechanisms of that feedback process are poorly understood. We assessed the temporal characteristics of glucocorticoid-negative feedback in vivo using a procedure for drug infusions and serial blood collection in unanesthetized rats that produced a minimal disruption of basal ACTH plasma levels. We compared the negative feedback effectiveness present when stress onset coincides with corticosterone's (CORT) rapidly rising phase (30 sec pretreatment), high plateau phase (15 min pretreatment), or restored basal phase (60 min pretreatment) as well as effectiveness when CORT infusion occurs after the onset of stress (5 min poststress onset). CORT treatment prior to stress onset acted remarkably fast (within 30 sec) to suppress stress-induced ACTH secretion. Furthermore, fast feedback induction did not require rapid increases in CORT at the time of stress onset (hormone rate independent), and those feedback actions were relatively long lasting (≥15 min). In contrast, CORT elevation after stress onset produced limited and delayed ACTH suppression (stress state resistance). There was a parallel stress-state resistance for CORT inhibition of stress-induced Crh heteronuclear RNA in the paraventricular nucleus but not Pomc heteronuclear RNA in the anterior pituitary. CORT treatment did not suppress stress-induced prolactin secretion, suggesting that CORT feedback is restricted to the control of hypothalamic-pituitary-adrenal axis elements of a stress response. These temporal, stress-state, and system-level features of in vivo CORT feedback provide an important physiological context for ex vivo studies of molecular and cellular mechanisms of CORT-negative feedback.</description><identifier>ISSN: 0013-7227</identifier><identifier>EISSN: 1945-7170</identifier><identifier>DOI: 10.1210/en.2016-1123</identifier><identifier>PMID: 27145013</identifier><language>eng</language><publisher>United States: Endocrine Society</publisher><subject>Adrenalectomy ; Adrenocorticotropic hormone ; Adrenocorticotropic Hormone - secretion ; Animals ; Blood levels ; Corticosterone ; Corticosterone - pharmacology ; Corticotropin-Releasing Hormone - metabolism ; Effectiveness ; Feedback inhibition ; Feedback, Physiological - drug effects ; Glucocorticoids ; Hypothalamic-pituitary-adrenal axis ; Hypothalamo-Hypophyseal System - drug effects ; Hypothalamo-Hypophyseal System - metabolism ; Hypothalamo-Hypophyseal System - physiopathology ; Hypothalamus ; In vivo methods and tests ; Male ; Negative feedback ; Original Research ; Paraventricular Hypothalamic Nucleus - metabolism ; Paraventricular nucleus ; Physiology ; Pituitary (anterior) ; Pituitary-Adrenal System - drug effects ; Pituitary-Adrenal System - metabolism ; Pituitary-Adrenal System - physiopathology ; Plasma levels ; Pretreatment ; Prolactin ; Rats ; Rats, Sprague-Dawley ; Restraint, Physical ; Secretion ; Stress response ; Stress, Physiological - drug effects ; Stress, Physiological - physiology ; Stress, Psychological - metabolism ; Stress, Psychological - physiopathology</subject><ispartof>Endocrinology (Philadelphia), 2016-07, Vol.157 (7), p.2785-2798</ispartof><rights>Copyright © 2016 by the Endocrine Society</rights><rights>Copyright © 2016 by the Endocrine Society 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c521t-eb2cb229477a3b8020eb70e6f0f2bfcfefbec9c709894fca8796cb9c985d65873</citedby><cites>FETCH-LOGICAL-c521t-eb2cb229477a3b8020eb70e6f0f2bfcfefbec9c709894fca8796cb9c985d65873</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27145013$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Osterlund, Chad D</creatorcontrib><creatorcontrib>Rodriguez-Santiago, Mariana</creatorcontrib><creatorcontrib>Woodruff, Elizabeth R</creatorcontrib><creatorcontrib>Newsom, Ryan J</creatorcontrib><creatorcontrib>Chadayammuri, Anjali P</creatorcontrib><creatorcontrib>Spencer, Robert L</creatorcontrib><title>Glucocorticoid Fast Feedback Inhibition of Stress-Induced ACTH Secretion in the Male Rat: Rate Independence and Stress-State Resistance</title><title>Endocrinology (Philadelphia)</title><addtitle>Endocrinology</addtitle><description>Normal glucocorticoid secretion is critical for physiological and mental health. Glucocorticoid secretion is dynamically regulated by glucocorticoid-negative feedback; however, the mechanisms of that feedback process are poorly understood. We assessed the temporal characteristics of glucocorticoid-negative feedback in vivo using a procedure for drug infusions and serial blood collection in unanesthetized rats that produced a minimal disruption of basal ACTH plasma levels. We compared the negative feedback effectiveness present when stress onset coincides with corticosterone's (CORT) rapidly rising phase (30 sec pretreatment), high plateau phase (15 min pretreatment), or restored basal phase (60 min pretreatment) as well as effectiveness when CORT infusion occurs after the onset of stress (5 min poststress onset). CORT treatment prior to stress onset acted remarkably fast (within 30 sec) to suppress stress-induced ACTH secretion. Furthermore, fast feedback induction did not require rapid increases in CORT at the time of stress onset (hormone rate independent), and those feedback actions were relatively long lasting (≥15 min). In contrast, CORT elevation after stress onset produced limited and delayed ACTH suppression (stress state resistance). There was a parallel stress-state resistance for CORT inhibition of stress-induced Crh heteronuclear RNA in the paraventricular nucleus but not Pomc heteronuclear RNA in the anterior pituitary. CORT treatment did not suppress stress-induced prolactin secretion, suggesting that CORT feedback is restricted to the control of hypothalamic-pituitary-adrenal axis elements of a stress response. These temporal, stress-state, and system-level features of in vivo CORT feedback provide an important physiological context for ex vivo studies of molecular and cellular mechanisms of CORT-negative feedback.</description><subject>Adrenalectomy</subject><subject>Adrenocorticotropic hormone</subject><subject>Adrenocorticotropic Hormone - secretion</subject><subject>Animals</subject><subject>Blood levels</subject><subject>Corticosterone</subject><subject>Corticosterone - pharmacology</subject><subject>Corticotropin-Releasing Hormone - metabolism</subject><subject>Effectiveness</subject><subject>Feedback inhibition</subject><subject>Feedback, Physiological - drug effects</subject><subject>Glucocorticoids</subject><subject>Hypothalamic-pituitary-adrenal axis</subject><subject>Hypothalamo-Hypophyseal System - drug effects</subject><subject>Hypothalamo-Hypophyseal System - metabolism</subject><subject>Hypothalamo-Hypophyseal System - physiopathology</subject><subject>Hypothalamus</subject><subject>In vivo methods and tests</subject><subject>Male</subject><subject>Negative feedback</subject><subject>Original Research</subject><subject>Paraventricular Hypothalamic Nucleus - metabolism</subject><subject>Paraventricular nucleus</subject><subject>Physiology</subject><subject>Pituitary (anterior)</subject><subject>Pituitary-Adrenal System - drug effects</subject><subject>Pituitary-Adrenal System - metabolism</subject><subject>Pituitary-Adrenal System - physiopathology</subject><subject>Plasma levels</subject><subject>Pretreatment</subject><subject>Prolactin</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Restraint, Physical</subject><subject>Secretion</subject><subject>Stress response</subject><subject>Stress, Physiological - drug effects</subject><subject>Stress, Physiological - physiology</subject><subject>Stress, Psychological - metabolism</subject><subject>Stress, Psychological - physiopathology</subject><issn>0013-7227</issn><issn>1945-7170</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><recordid>eNqNkl1rFDEUhgdR7Fq981oCXuiFU_M1k4kXQlncdqEidOt1yGTOuKmzyZhkBH-Bf9tMd1s_UPDmhHAeHk7ynqJ4SvAJoQS_BndCMalLQii7VyyI5FUpiMD3iwXGhJWCUnFUPIrxOl855-xhcUQF4VVuLorvZ8NkvPEhWeNth1Y6JrQC6FptPqO129rWJusd8j3apAAxlmvXTQY6dLq8OkcbMAFuAOtQ2gJ6rwdAlzq9mQtkQwcj5OIMIO26W8kmzd1LiDYmnXuPiwe9HiI8OZzHxcfVu6vleXnx4Wy9PL0oTUVJKqGlpqVUciE0axtMMbQCQ93jnra96aFvwUgjsGwk741uhKxNK41sqq6uGsGOi7d77zi1O-gMuBT0oMZgdzp8U15b9XvH2a365L8qLqmsKp4FLw-C4L9MEJPa2WhgGLQDP0VFGkmahjZU_geaA6Gc31if_4Fe-ym4_BOKEYYFYTVjmXq1p0zwMQbo7-YmWM3LoMCpeRnUvAwZf_brW-_g2_Qz8GIP-Gn8l6o8qNiezFF6E6yDcY7x55R_HeAHMETNmg</recordid><startdate>20160701</startdate><enddate>20160701</enddate><creator>Osterlund, Chad D</creator><creator>Rodriguez-Santiago, Mariana</creator><creator>Woodruff, Elizabeth R</creator><creator>Newsom, Ryan J</creator><creator>Chadayammuri, Anjali P</creator><creator>Spencer, Robert L</creator><general>Endocrine Society</general><general>Oxford University Press</general><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>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160701</creationdate><title>Glucocorticoid Fast Feedback Inhibition of Stress-Induced ACTH Secretion in the Male Rat: Rate Independence and Stress-State Resistance</title><author>Osterlund, Chad D ; Rodriguez-Santiago, Mariana ; Woodruff, Elizabeth R ; Newsom, Ryan J ; Chadayammuri, Anjali P ; Spencer, Robert L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c521t-eb2cb229477a3b8020eb70e6f0f2bfcfefbec9c709894fca8796cb9c985d65873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adrenalectomy</topic><topic>Adrenocorticotropic hormone</topic><topic>Adrenocorticotropic Hormone - secretion</topic><topic>Animals</topic><topic>Blood levels</topic><topic>Corticosterone</topic><topic>Corticosterone - pharmacology</topic><topic>Corticotropin-Releasing Hormone - metabolism</topic><topic>Effectiveness</topic><topic>Feedback inhibition</topic><topic>Feedback, Physiological - drug effects</topic><topic>Glucocorticoids</topic><topic>Hypothalamic-pituitary-adrenal axis</topic><topic>Hypothalamo-Hypophyseal System - drug effects</topic><topic>Hypothalamo-Hypophyseal System - metabolism</topic><topic>Hypothalamo-Hypophyseal System - physiopathology</topic><topic>Hypothalamus</topic><topic>In vivo methods and tests</topic><topic>Male</topic><topic>Negative feedback</topic><topic>Original Research</topic><topic>Paraventricular Hypothalamic Nucleus - metabolism</topic><topic>Paraventricular nucleus</topic><topic>Physiology</topic><topic>Pituitary (anterior)</topic><topic>Pituitary-Adrenal System - drug effects</topic><topic>Pituitary-Adrenal System - metabolism</topic><topic>Pituitary-Adrenal System - physiopathology</topic><topic>Plasma levels</topic><topic>Pretreatment</topic><topic>Prolactin</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Restraint, Physical</topic><topic>Secretion</topic><topic>Stress response</topic><topic>Stress, Physiological - drug effects</topic><topic>Stress, Physiological - physiology</topic><topic>Stress, Psychological - metabolism</topic><topic>Stress, Psychological - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Osterlund, Chad D</creatorcontrib><creatorcontrib>Rodriguez-Santiago, Mariana</creatorcontrib><creatorcontrib>Woodruff, Elizabeth R</creatorcontrib><creatorcontrib>Newsom, Ryan J</creatorcontrib><creatorcontrib>Chadayammuri, Anjali P</creatorcontrib><creatorcontrib>Spencer, Robert L</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Endocrinology (Philadelphia)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Osterlund, Chad D</au><au>Rodriguez-Santiago, Mariana</au><au>Woodruff, Elizabeth R</au><au>Newsom, Ryan J</au><au>Chadayammuri, Anjali P</au><au>Spencer, Robert L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Glucocorticoid Fast Feedback Inhibition of Stress-Induced ACTH Secretion in the Male Rat: Rate Independence and Stress-State Resistance</atitle><jtitle>Endocrinology (Philadelphia)</jtitle><addtitle>Endocrinology</addtitle><date>2016-07-01</date><risdate>2016</risdate><volume>157</volume><issue>7</issue><spage>2785</spage><epage>2798</epage><pages>2785-2798</pages><issn>0013-7227</issn><eissn>1945-7170</eissn><abstract>Normal glucocorticoid secretion is critical for physiological and mental health. Glucocorticoid secretion is dynamically regulated by glucocorticoid-negative feedback; however, the mechanisms of that feedback process are poorly understood. We assessed the temporal characteristics of glucocorticoid-negative feedback in vivo using a procedure for drug infusions and serial blood collection in unanesthetized rats that produced a minimal disruption of basal ACTH plasma levels. We compared the negative feedback effectiveness present when stress onset coincides with corticosterone's (CORT) rapidly rising phase (30 sec pretreatment), high plateau phase (15 min pretreatment), or restored basal phase (60 min pretreatment) as well as effectiveness when CORT infusion occurs after the onset of stress (5 min poststress onset). CORT treatment prior to stress onset acted remarkably fast (within 30 sec) to suppress stress-induced ACTH secretion. Furthermore, fast feedback induction did not require rapid increases in CORT at the time of stress onset (hormone rate independent), and those feedback actions were relatively long lasting (≥15 min). In contrast, CORT elevation after stress onset produced limited and delayed ACTH suppression (stress state resistance). There was a parallel stress-state resistance for CORT inhibition of stress-induced Crh heteronuclear RNA in the paraventricular nucleus but not Pomc heteronuclear RNA in the anterior pituitary. CORT treatment did not suppress stress-induced prolactin secretion, suggesting that CORT feedback is restricted to the control of hypothalamic-pituitary-adrenal axis elements of a stress response. These temporal, stress-state, and system-level features of in vivo CORT feedback provide an important physiological context for ex vivo studies of molecular and cellular mechanisms of CORT-negative feedback.</abstract><cop>United States</cop><pub>Endocrine Society</pub><pmid>27145013</pmid><doi>10.1210/en.2016-1123</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 0013-7227
ispartof Endocrinology (Philadelphia), 2016-07, Vol.157 (7), p.2785-2798
issn 0013-7227
1945-7170
language eng
recordid cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4929554
source Oxford University Press:Jisc Collections:OUP Read and Publish 2024-2025 (2024 collection) (Reading list)
subjects Adrenalectomy
Adrenocorticotropic hormone
Adrenocorticotropic Hormone - secretion
Animals
Blood levels
Corticosterone
Corticosterone - pharmacology
Corticotropin-Releasing Hormone - metabolism
Effectiveness
Feedback inhibition
Feedback, Physiological - drug effects
Glucocorticoids
Hypothalamic-pituitary-adrenal axis
Hypothalamo-Hypophyseal System - drug effects
Hypothalamo-Hypophyseal System - metabolism
Hypothalamo-Hypophyseal System - physiopathology
Hypothalamus
In vivo methods and tests
Male
Negative feedback
Original Research
Paraventricular Hypothalamic Nucleus - metabolism
Paraventricular nucleus
Physiology
Pituitary (anterior)
Pituitary-Adrenal System - drug effects
Pituitary-Adrenal System - metabolism
Pituitary-Adrenal System - physiopathology
Plasma levels
Pretreatment
Prolactin
Rats
Rats, Sprague-Dawley
Restraint, Physical
Secretion
Stress response
Stress, Physiological - drug effects
Stress, Physiological - physiology
Stress, Psychological - metabolism
Stress, Psychological - physiopathology
title Glucocorticoid Fast Feedback Inhibition of Stress-Induced ACTH Secretion in the Male Rat: Rate Independence and Stress-State Resistance
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-31T23%3A10%3A34IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Glucocorticoid%20Fast%20Feedback%20Inhibition%20of%20Stress-Induced%20ACTH%20Secretion%20in%20the%20Male%20Rat:%20Rate%20Independence%20and%20Stress-State%20Resistance&rft.jtitle=Endocrinology%20(Philadelphia)&rft.au=Osterlund,%20Chad%20D&rft.date=2016-07-01&rft.volume=157&rft.issue=7&rft.spage=2785&rft.epage=2798&rft.pages=2785-2798&rft.issn=0013-7227&rft.eissn=1945-7170&rft_id=info:doi/10.1210/en.2016-1123&rft_dat=%3Cproquest_pubme%3E1891882829%3C/proquest_pubme%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c521t-eb2cb229477a3b8020eb70e6f0f2bfcfefbec9c709894fca8796cb9c985d65873%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=3130713633&rft_id=info:pmid/27145013&rft_oup_id=10.1210/en.2016-1123&rfr_iscdi=true