Alterations in hypothalamic–pituitary–adrenal axis activity and in levels of proopiomelanocortin and corticotropin-releasing hormone-receptor 1 mRNAs in the pituitary and hypothalamus of the rat during chronic ‘binge’ cocaine and withdrawal

Tolerance to the stimulatory effects of cocaine on the hypothalamic–pituitary–adrenal (HPA) axis develops after chronic ‘binge’ cocaine exposure in the rat. This blunting of HPA axis activity in response to cocaine is associated with a cocaine-induced reduction of corticotropin-releasing hormone (CR...

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Veröffentlicht in:Brain research 2003-02, Vol.964 (2), p.187-199
Hauptverfasser: Zhou, Yan, Spangler, Rudolph, Schlussman, Stefan D, Ho, Ann, Kreek, Mary Jeanne
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Spangler, Rudolph
Schlussman, Stefan D
Ho, Ann
Kreek, Mary Jeanne
description Tolerance to the stimulatory effects of cocaine on the hypothalamic–pituitary–adrenal (HPA) axis develops after chronic ‘binge’ cocaine exposure in the rat. This blunting of HPA axis activity in response to cocaine is associated with a cocaine-induced reduction of corticotropin-releasing hormone (CRH) mRNA level in the hypothalamus. There is limited information about the effects of withdrawal from chronic cocaine on HPA activity. The present studies were undertaken to determine levels of the HPA hormones adrenocorticotropic hormone (ACTH) and corticosterone across 10 days of withdrawal following chronic ‘binge’ pattern cocaine administration (3×15 mg/kg/day at hourly intervals) for 14 days. Male Fischer rats showed a significantly attenuated HPA axis response to chronic ‘binge’ pattern cocaine administration 30 min after the last injection on the 14th day, as measured by both plasma ACTH and corticosterone levels at the nadir time point. Twenty-four hours following the final administration of ‘binge’ cocaine (the 1st day of withdrawal), a significant elevation of plasma ACTH levels and a modest, but significant, elevation of plasma corticosterone levels were found at the nadir time point. This acute withdrawal-related activation of the hormones of the HPA axis was no longer found on the 10th day of withdrawal. In the anterior pituitary, levels of both proopiomelanocortin (POMC) and CRH-receptor 1 (R1) mRNAs were significantly higher than saline controls on the 14th day of chronic ‘binge’ cocaine and were at control levels on the 4th day of withdrawal. In the neurointermediate lobe of the pituitary, a sustained reduction in POMC mRNA levels was observed on the 3rd, 7th and 14th day of chronic ‘binge’ cocaine, but POMC mRNA was at control levels by the 4th day of withdrawal. In the hypothalamus, POMC mRNA levels showed a transient decrease on the 1st day of ‘binge’ cocaine with no change during chronic ‘binge’ cocaine or its withdrawal. CRH mRNA levels in the hypothalamus were not different from saline controls on the 1st and 4th days of withdrawal. Taken together, the present results show that after development of adaptation or tolerance to chronic ‘binge’ cocaine there is an increase in HPA activity during acute cocaine withdrawal. In addition to being associated with CRH input from the hypothalamus, the activation of the HPA axis by cocaine withdrawal may be, at least in part, due to the increased POMC and/or CRH-R1 gene expression observed in the anterio
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This blunting of HPA axis activity in response to cocaine is associated with a cocaine-induced reduction of corticotropin-releasing hormone (CRH) mRNA level in the hypothalamus. There is limited information about the effects of withdrawal from chronic cocaine on HPA activity. The present studies were undertaken to determine levels of the HPA hormones adrenocorticotropic hormone (ACTH) and corticosterone across 10 days of withdrawal following chronic ‘binge’ pattern cocaine administration (3×15 mg/kg/day at hourly intervals) for 14 days. Male Fischer rats showed a significantly attenuated HPA axis response to chronic ‘binge’ pattern cocaine administration 30 min after the last injection on the 14th day, as measured by both plasma ACTH and corticosterone levels at the nadir time point. Twenty-four hours following the final administration of ‘binge’ cocaine (the 1st day of withdrawal), a significant elevation of plasma ACTH levels and a modest, but significant, elevation of plasma corticosterone levels were found at the nadir time point. This acute withdrawal-related activation of the hormones of the HPA axis was no longer found on the 10th day of withdrawal. In the anterior pituitary, levels of both proopiomelanocortin (POMC) and CRH-receptor 1 (R1) mRNAs were significantly higher than saline controls on the 14th day of chronic ‘binge’ cocaine and were at control levels on the 4th day of withdrawal. In the neurointermediate lobe of the pituitary, a sustained reduction in POMC mRNA levels was observed on the 3rd, 7th and 14th day of chronic ‘binge’ cocaine, but POMC mRNA was at control levels by the 4th day of withdrawal. In the hypothalamus, POMC mRNA levels showed a transient decrease on the 1st day of ‘binge’ cocaine with no change during chronic ‘binge’ cocaine or its withdrawal. CRH mRNA levels in the hypothalamus were not different from saline controls on the 1st and 4th days of withdrawal. Taken together, the present results show that after development of adaptation or tolerance to chronic ‘binge’ cocaine there is an increase in HPA activity during acute cocaine withdrawal. In addition to being associated with CRH input from the hypothalamus, the activation of the HPA axis by cocaine withdrawal may be, at least in part, due to the increased POMC and/or CRH-R1 gene expression observed in the anterior pituitary after chronic ‘binge’ cocaine.</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/S0006-8993(02)03929-X</identifier><identifier>PMID: 12576179</identifier><identifier>CODEN: BRREAP</identifier><language>eng</language><publisher>London: Elsevier B.V</publisher><subject>ACTH ; Adrenal Glands - drug effects ; Adrenal Glands - metabolism ; Adrenocorticotropic Hormone - metabolism ; Amygdala - drug effects ; Amygdala - metabolism ; Animals ; Anterior pituitary ; Biological and medical sciences ; Blotting, Northern ; Chronic ‘binge’ cocaine ; Cocaine - administration &amp; dosage ; Cocaine - pharmacology ; Cocaine withdrawal ; Corticosterone ; Corticosterone - metabolism ; Corticotropin-Releasing Hormone - drug effects ; Corticotropin-Releasing Hormone - metabolism ; CRH-R1 ; Dopamine Uptake Inhibitors - administration &amp; dosage ; Dopamine Uptake Inhibitors - pharmacology ; Enkephalins - metabolism ; Frontal Lobe - drug effects ; Frontal Lobe - metabolism ; Hypothalamic–pituitary–adrenal axis ; Hypothalamo-Hypophyseal System - drug effects ; Hypothalamo-Hypophyseal System - metabolism ; Male ; Medical sciences ; Neuropharmacology ; Pharmacology. Drug treatments ; Pituitary Gland - drug effects ; Pituitary Gland - metabolism ; Pituitary-Adrenal System - drug effects ; Pituitary-Adrenal System - metabolism ; POMC ; Pro-Opiomelanocortin - drug effects ; Pro-Opiomelanocortin - metabolism ; Protein Precursors - metabolism ; Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease) ; Psychology. Psychoanalysis. Psychiatry ; Psychopharmacology ; Radioimmunoassay ; Rats ; Rats, Inbred F344 ; Receptors, Corticotropin-Releasing Hormone - drug effects ; Receptors, Corticotropin-Releasing Hormone - genetics ; Receptors, Corticotropin-Releasing Hormone - metabolism ; RNA, Messenger - metabolism ; Substance Withdrawal Syndrome - metabolism ; Time Factors</subject><ispartof>Brain research, 2003-02, Vol.964 (2), p.187-199</ispartof><rights>2002 Elsevier Science B.V.</rights><rights>2003 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c422t-79526e52309c7f60c2d50cd71ade6247da5f40d891246645c7523f23e0519e6c3</citedby><cites>FETCH-LOGICAL-c422t-79526e52309c7f60c2d50cd71ade6247da5f40d891246645c7523f23e0519e6c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0006-8993(02)03929-X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,777,781,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=14506655$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12576179$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhou, Yan</creatorcontrib><creatorcontrib>Spangler, Rudolph</creatorcontrib><creatorcontrib>Schlussman, Stefan D</creatorcontrib><creatorcontrib>Ho, Ann</creatorcontrib><creatorcontrib>Kreek, Mary Jeanne</creatorcontrib><title>Alterations in hypothalamic–pituitary–adrenal axis activity and in levels of proopiomelanocortin and corticotropin-releasing hormone-receptor 1 mRNAs in the pituitary and hypothalamus of the rat during chronic ‘binge’ cocaine and withdrawal</title><title>Brain research</title><addtitle>Brain Res</addtitle><description>Tolerance to the stimulatory effects of cocaine on the hypothalamic–pituitary–adrenal (HPA) axis develops after chronic ‘binge’ cocaine exposure in the rat. This blunting of HPA axis activity in response to cocaine is associated with a cocaine-induced reduction of corticotropin-releasing hormone (CRH) mRNA level in the hypothalamus. There is limited information about the effects of withdrawal from chronic cocaine on HPA activity. The present studies were undertaken to determine levels of the HPA hormones adrenocorticotropic hormone (ACTH) and corticosterone across 10 days of withdrawal following chronic ‘binge’ pattern cocaine administration (3×15 mg/kg/day at hourly intervals) for 14 days. Male Fischer rats showed a significantly attenuated HPA axis response to chronic ‘binge’ pattern cocaine administration 30 min after the last injection on the 14th day, as measured by both plasma ACTH and corticosterone levels at the nadir time point. Twenty-four hours following the final administration of ‘binge’ cocaine (the 1st day of withdrawal), a significant elevation of plasma ACTH levels and a modest, but significant, elevation of plasma corticosterone levels were found at the nadir time point. This acute withdrawal-related activation of the hormones of the HPA axis was no longer found on the 10th day of withdrawal. In the anterior pituitary, levels of both proopiomelanocortin (POMC) and CRH-receptor 1 (R1) mRNAs were significantly higher than saline controls on the 14th day of chronic ‘binge’ cocaine and were at control levels on the 4th day of withdrawal. In the neurointermediate lobe of the pituitary, a sustained reduction in POMC mRNA levels was observed on the 3rd, 7th and 14th day of chronic ‘binge’ cocaine, but POMC mRNA was at control levels by the 4th day of withdrawal. In the hypothalamus, POMC mRNA levels showed a transient decrease on the 1st day of ‘binge’ cocaine with no change during chronic ‘binge’ cocaine or its withdrawal. CRH mRNA levels in the hypothalamus were not different from saline controls on the 1st and 4th days of withdrawal. Taken together, the present results show that after development of adaptation or tolerance to chronic ‘binge’ cocaine there is an increase in HPA activity during acute cocaine withdrawal. In addition to being associated with CRH input from the hypothalamus, the activation of the HPA axis by cocaine withdrawal may be, at least in part, due to the increased POMC and/or CRH-R1 gene expression observed in the anterior pituitary after chronic ‘binge’ cocaine.</description><subject>ACTH</subject><subject>Adrenal Glands - drug effects</subject><subject>Adrenal Glands - metabolism</subject><subject>Adrenocorticotropic Hormone - metabolism</subject><subject>Amygdala - drug effects</subject><subject>Amygdala - metabolism</subject><subject>Animals</subject><subject>Anterior pituitary</subject><subject>Biological and medical sciences</subject><subject>Blotting, Northern</subject><subject>Chronic ‘binge’ cocaine</subject><subject>Cocaine - administration &amp; dosage</subject><subject>Cocaine - pharmacology</subject><subject>Cocaine withdrawal</subject><subject>Corticosterone</subject><subject>Corticosterone - metabolism</subject><subject>Corticotropin-Releasing Hormone - drug effects</subject><subject>Corticotropin-Releasing Hormone - metabolism</subject><subject>CRH-R1</subject><subject>Dopamine Uptake Inhibitors - administration &amp; dosage</subject><subject>Dopamine Uptake Inhibitors - pharmacology</subject><subject>Enkephalins - metabolism</subject><subject>Frontal Lobe - drug effects</subject><subject>Frontal Lobe - metabolism</subject><subject>Hypothalamic–pituitary–adrenal axis</subject><subject>Hypothalamo-Hypophyseal System - drug effects</subject><subject>Hypothalamo-Hypophyseal System - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Neuropharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Pituitary Gland - drug effects</subject><subject>Pituitary Gland - metabolism</subject><subject>Pituitary-Adrenal System - drug effects</subject><subject>Pituitary-Adrenal System - metabolism</subject><subject>POMC</subject><subject>Pro-Opiomelanocortin - drug effects</subject><subject>Pro-Opiomelanocortin - metabolism</subject><subject>Protein Precursors - metabolism</subject><subject>Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease)</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopharmacology</subject><subject>Radioimmunoassay</subject><subject>Rats</subject><subject>Rats, Inbred F344</subject><subject>Receptors, Corticotropin-Releasing Hormone - drug effects</subject><subject>Receptors, Corticotropin-Releasing Hormone - genetics</subject><subject>Receptors, Corticotropin-Releasing Hormone - metabolism</subject><subject>RNA, Messenger - metabolism</subject><subject>Substance Withdrawal Syndrome - metabolism</subject><subject>Time Factors</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1u1DAQxyMEotvCI4B8AZVDwHYSZ3NCq4ovqQKJD6k3y7UnxMixU9vZsrd9By7wevsUHHGyq-6Rk8ee38z8Pf8se0LwS4IJe_UFY8zyZdMU55i-wEVDm_zqXrYgy5rmjJb4fra4Q06y0xB-pGtRNPhhdkJoVTNSN4vs78pE8CJqZwPSFnWbwcVOGNFrudv-GnQcdRR-k2KhPFhhkPipAxIy6rWOGySsmuoMrMEE5Fo0eOcG7XowwjrpfEzZCZpD6aJPWZt7MCCCtt9R53zvLKQXCUN0HhHUf_64mtXEDtCdhLnLUd84T5uIJB-p0U_NZOed1RLttr-v0x122z9psBTawlx-q2OnvLgV5lH2oBUmwOPDeZZ9e_vm68X7_PLTuw8Xq8tclpTGvG4qyqCiBW5k3TIsqaqwVDURCtKWayWqtsRq2RBaMlZWsk5sSwvAFWmAyeIse77vm_ZyM0KIvNdBgknbATcGTpYsOdQUCaz2oPQuBA8tH7zu0785wXyynM-W88lPjimfLedXqe7pYcB43YM6Vh08TsCzAyCCFKb1wkodjlxZYcaqKnGv91wyEtYaPA9Sg5WgdPImcuX0f6T8A-wc1BM</recordid><startdate>20030228</startdate><enddate>20030228</enddate><creator>Zhou, Yan</creator><creator>Spangler, Rudolph</creator><creator>Schlussman, Stefan D</creator><creator>Ho, Ann</creator><creator>Kreek, Mary Jeanne</creator><general>Elsevier B.V</general><general>Elsevier</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></search><sort><creationdate>20030228</creationdate><title>Alterations in hypothalamic–pituitary–adrenal axis activity and in levels of proopiomelanocortin and corticotropin-releasing hormone-receptor 1 mRNAs in the pituitary and hypothalamus of the rat during chronic ‘binge’ cocaine and withdrawal</title><author>Zhou, Yan ; Spangler, Rudolph ; Schlussman, Stefan D ; Ho, Ann ; Kreek, Mary Jeanne</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c422t-79526e52309c7f60c2d50cd71ade6247da5f40d891246645c7523f23e0519e6c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>ACTH</topic><topic>Adrenal Glands - drug effects</topic><topic>Adrenal Glands - metabolism</topic><topic>Adrenocorticotropic Hormone - metabolism</topic><topic>Amygdala - drug effects</topic><topic>Amygdala - metabolism</topic><topic>Animals</topic><topic>Anterior pituitary</topic><topic>Biological and medical sciences</topic><topic>Blotting, Northern</topic><topic>Chronic ‘binge’ cocaine</topic><topic>Cocaine - administration &amp; dosage</topic><topic>Cocaine - pharmacology</topic><topic>Cocaine withdrawal</topic><topic>Corticosterone</topic><topic>Corticosterone - metabolism</topic><topic>Corticotropin-Releasing Hormone - drug effects</topic><topic>Corticotropin-Releasing Hormone - metabolism</topic><topic>CRH-R1</topic><topic>Dopamine Uptake Inhibitors - administration &amp; dosage</topic><topic>Dopamine Uptake Inhibitors - pharmacology</topic><topic>Enkephalins - metabolism</topic><topic>Frontal Lobe - drug effects</topic><topic>Frontal Lobe - metabolism</topic><topic>Hypothalamic–pituitary–adrenal axis</topic><topic>Hypothalamo-Hypophyseal System - drug effects</topic><topic>Hypothalamo-Hypophyseal System - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Neuropharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Pituitary Gland - drug effects</topic><topic>Pituitary Gland - metabolism</topic><topic>Pituitary-Adrenal System - drug effects</topic><topic>Pituitary-Adrenal System - metabolism</topic><topic>POMC</topic><topic>Pro-Opiomelanocortin - drug effects</topic><topic>Pro-Opiomelanocortin - metabolism</topic><topic>Protein Precursors - metabolism</topic><topic>Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease)</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopharmacology</topic><topic>Radioimmunoassay</topic><topic>Rats</topic><topic>Rats, Inbred F344</topic><topic>Receptors, Corticotropin-Releasing Hormone - drug effects</topic><topic>Receptors, Corticotropin-Releasing Hormone - genetics</topic><topic>Receptors, Corticotropin-Releasing Hormone - metabolism</topic><topic>RNA, Messenger - metabolism</topic><topic>Substance Withdrawal Syndrome - metabolism</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhou, Yan</creatorcontrib><creatorcontrib>Spangler, Rudolph</creatorcontrib><creatorcontrib>Schlussman, Stefan D</creatorcontrib><creatorcontrib>Ho, Ann</creatorcontrib><creatorcontrib>Kreek, Mary Jeanne</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><jtitle>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhou, Yan</au><au>Spangler, Rudolph</au><au>Schlussman, Stefan D</au><au>Ho, Ann</au><au>Kreek, Mary Jeanne</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Alterations in hypothalamic–pituitary–adrenal axis activity and in levels of proopiomelanocortin and corticotropin-releasing hormone-receptor 1 mRNAs in the pituitary and hypothalamus of the rat during chronic ‘binge’ cocaine and withdrawal</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>2003-02-28</date><risdate>2003</risdate><volume>964</volume><issue>2</issue><spage>187</spage><epage>199</epage><pages>187-199</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><coden>BRREAP</coden><abstract>Tolerance to the stimulatory effects of cocaine on the hypothalamic–pituitary–adrenal (HPA) axis develops after chronic ‘binge’ cocaine exposure in the rat. This blunting of HPA axis activity in response to cocaine is associated with a cocaine-induced reduction of corticotropin-releasing hormone (CRH) mRNA level in the hypothalamus. There is limited information about the effects of withdrawal from chronic cocaine on HPA activity. The present studies were undertaken to determine levels of the HPA hormones adrenocorticotropic hormone (ACTH) and corticosterone across 10 days of withdrawal following chronic ‘binge’ pattern cocaine administration (3×15 mg/kg/day at hourly intervals) for 14 days. Male Fischer rats showed a significantly attenuated HPA axis response to chronic ‘binge’ pattern cocaine administration 30 min after the last injection on the 14th day, as measured by both plasma ACTH and corticosterone levels at the nadir time point. Twenty-four hours following the final administration of ‘binge’ cocaine (the 1st day of withdrawal), a significant elevation of plasma ACTH levels and a modest, but significant, elevation of plasma corticosterone levels were found at the nadir time point. This acute withdrawal-related activation of the hormones of the HPA axis was no longer found on the 10th day of withdrawal. In the anterior pituitary, levels of both proopiomelanocortin (POMC) and CRH-receptor 1 (R1) mRNAs were significantly higher than saline controls on the 14th day of chronic ‘binge’ cocaine and were at control levels on the 4th day of withdrawal. In the neurointermediate lobe of the pituitary, a sustained reduction in POMC mRNA levels was observed on the 3rd, 7th and 14th day of chronic ‘binge’ cocaine, but POMC mRNA was at control levels by the 4th day of withdrawal. In the hypothalamus, POMC mRNA levels showed a transient decrease on the 1st day of ‘binge’ cocaine with no change during chronic ‘binge’ cocaine or its withdrawal. CRH mRNA levels in the hypothalamus were not different from saline controls on the 1st and 4th days of withdrawal. Taken together, the present results show that after development of adaptation or tolerance to chronic ‘binge’ cocaine there is an increase in HPA activity during acute cocaine withdrawal. In addition to being associated with CRH input from the hypothalamus, the activation of the HPA axis by cocaine withdrawal may be, at least in part, due to the increased POMC and/or CRH-R1 gene expression observed in the anterior pituitary after chronic ‘binge’ cocaine.</abstract><cop>London</cop><cop>Amsterdam</cop><cop>New York, NY</cop><pub>Elsevier B.V</pub><pmid>12576179</pmid><doi>10.1016/S0006-8993(02)03929-X</doi><tpages>13</tpages></addata></record>
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subjects ACTH
Adrenal Glands - drug effects
Adrenal Glands - metabolism
Adrenocorticotropic Hormone - metabolism
Amygdala - drug effects
Amygdala - metabolism
Animals
Anterior pituitary
Biological and medical sciences
Blotting, Northern
Chronic ‘binge’ cocaine
Cocaine - administration & dosage
Cocaine - pharmacology
Cocaine withdrawal
Corticosterone
Corticosterone - metabolism
Corticotropin-Releasing Hormone - drug effects
Corticotropin-Releasing Hormone - metabolism
CRH-R1
Dopamine Uptake Inhibitors - administration & dosage
Dopamine Uptake Inhibitors - pharmacology
Enkephalins - metabolism
Frontal Lobe - drug effects
Frontal Lobe - metabolism
Hypothalamic–pituitary–adrenal axis
Hypothalamo-Hypophyseal System - drug effects
Hypothalamo-Hypophyseal System - metabolism
Male
Medical sciences
Neuropharmacology
Pharmacology. Drug treatments
Pituitary Gland - drug effects
Pituitary Gland - metabolism
Pituitary-Adrenal System - drug effects
Pituitary-Adrenal System - metabolism
POMC
Pro-Opiomelanocortin - drug effects
Pro-Opiomelanocortin - metabolism
Protein Precursors - metabolism
Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease)
Psychology. Psychoanalysis. Psychiatry
Psychopharmacology
Radioimmunoassay
Rats
Rats, Inbred F344
Receptors, Corticotropin-Releasing Hormone - drug effects
Receptors, Corticotropin-Releasing Hormone - genetics
Receptors, Corticotropin-Releasing Hormone - metabolism
RNA, Messenger - metabolism
Substance Withdrawal Syndrome - metabolism
Time Factors
title Alterations in hypothalamic–pituitary–adrenal axis activity and in levels of proopiomelanocortin and corticotropin-releasing hormone-receptor 1 mRNAs in the pituitary and hypothalamus of the rat during chronic ‘binge’ cocaine and withdrawal
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