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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...
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Published in: | Endocrinology (Philadelphia) 2016-07, Vol.157 (7), p.2785-2798 |
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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. |
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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 & 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 & 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> |
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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 |
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