Withdrawal-induced c-Fos expression in the rat centromedial amygdala 24 h following a single morphine exposure
An opiate antagonist was found to induce motivational withdrawal signs 24 h or even up to 48 h after a single dose of morphine in rats. The present study was undertaken to determine whether such a withdrawal state would modify the neuronal activity in the brain. A conditioned place aversion was esta...
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Veröffentlicht in: | Psychopharmacologia 2004-10, Vol.175 (4), p.428-435 |
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description | An opiate antagonist was found to induce motivational withdrawal signs 24 h or even up to 48 h after a single dose of morphine in rats.
The present study was undertaken to determine whether such a withdrawal state would modify the neuronal activity in the brain.
A conditioned place aversion was established following a one-trial paradigm in rats undergoing a single exposure to morphine (10 mg/kg) 24 h prior to naloxone administration (0.5 mg/kg). Subsequently, the expression of the protein product of c-fos gene (c-Fos) following naloxone administration was measured within the extended amygdala.
A significant increase in c-Fos immunoreactivity was seen in the centromedial amygdala (CMA), but not in the bed nucleus of the stria terminalis (BST) and the shell (AcbSh) of the nucleus accumbens (Acb) in rats treated with both morphine and naloxone. Further examination of the distribution of c-Fos-positive neurons along the rostrocaudal axis within CMA showed that the positive neurons distributed throughout this brain area and the caudal level of its central division (the central nucleus of the amygdala, CeA) exhibited the most robust labeling.
Neuronal activity can be increased by naloxone at a dose that produces conditioned place aversion 24 h after a single morphine exposure. CMA, particularly the caudal level of its central division, was of high sensitivity. The current data also suggest a possible involvement of CMA in negative motivational component of precipitated withdrawal from acute morphine dependence. |
doi_str_mv | 10.1007/s00213-004-1844-4 |
format | Article |
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The present study was undertaken to determine whether such a withdrawal state would modify the neuronal activity in the brain.
A conditioned place aversion was established following a one-trial paradigm in rats undergoing a single exposure to morphine (10 mg/kg) 24 h prior to naloxone administration (0.5 mg/kg). Subsequently, the expression of the protein product of c-fos gene (c-Fos) following naloxone administration was measured within the extended amygdala.
A significant increase in c-Fos immunoreactivity was seen in the centromedial amygdala (CMA), but not in the bed nucleus of the stria terminalis (BST) and the shell (AcbSh) of the nucleus accumbens (Acb) in rats treated with both morphine and naloxone. Further examination of the distribution of c-Fos-positive neurons along the rostrocaudal axis within CMA showed that the positive neurons distributed throughout this brain area and the caudal level of its central division (the central nucleus of the amygdala, CeA) exhibited the most robust labeling.
Neuronal activity can be increased by naloxone at a dose that produces conditioned place aversion 24 h after a single morphine exposure. CMA, particularly the caudal level of its central division, was of high sensitivity. The current data also suggest a possible involvement of CMA in negative motivational component of precipitated withdrawal from acute morphine dependence.</description><identifier>ISSN: 0033-3158</identifier><identifier>EISSN: 1432-2072</identifier><identifier>DOI: 10.1007/s00213-004-1844-4</identifier><identifier>PMID: 15175841</identifier><identifier>CODEN: PSYPAG</identifier><language>eng</language><publisher>Berlin: Springer</publisher><subject>Amygdala - metabolism ; Analgesics, Opioid - pharmacology ; Animals ; Biological and medical sciences ; Conditioning, Operant - drug effects ; Gene Expression - drug effects ; Genes, fos - drug effects ; Immunohistochemistry ; Male ; Medical sciences ; Morphine ; Morphine - pharmacology ; Naloxone - pharmacology ; Narcotic Antagonists - pharmacology ; Narcotics ; Neurons - drug effects ; Neurons - metabolism ; Neuropharmacology ; Pharmacology. Drug treatments ; Pharmacy ; Rats ; Rats, Sprague-Dawley ; Substance Withdrawal Syndrome - metabolism</subject><ispartof>Psychopharmacologia, 2004-10, Vol.175 (4), p.428-435</ispartof><rights>2004 INIST-CNRS</rights><rights>Copyright Springer-Verlag 2004</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c451t-78a65986ea8dc983edc48a37494c9139f479640a59489a69eea73d30316fcae93</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27915,27916</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16140676$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15175841$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>CHUNYU JIN</creatorcontrib><creatorcontrib>ARAKI, Hiroaki</creatorcontrib><creatorcontrib>NAGATA, Mari</creatorcontrib><creatorcontrib>SUEMARU, Katsuya</creatorcontrib><creatorcontrib>SHIBATA, Kazuhiko</creatorcontrib><creatorcontrib>KAWASAKI, Hiromu</creatorcontrib><creatorcontrib>HAMAMURA, Takashi</creatorcontrib><creatorcontrib>GOMITA, Yutaka</creatorcontrib><title>Withdrawal-induced c-Fos expression in the rat centromedial amygdala 24 h following a single morphine exposure</title><title>Psychopharmacologia</title><addtitle>Psychopharmacology (Berl)</addtitle><description>An opiate antagonist was found to induce motivational withdrawal signs 24 h or even up to 48 h after a single dose of morphine in rats.
The present study was undertaken to determine whether such a withdrawal state would modify the neuronal activity in the brain.
A conditioned place aversion was established following a one-trial paradigm in rats undergoing a single exposure to morphine (10 mg/kg) 24 h prior to naloxone administration (0.5 mg/kg). Subsequently, the expression of the protein product of c-fos gene (c-Fos) following naloxone administration was measured within the extended amygdala.
A significant increase in c-Fos immunoreactivity was seen in the centromedial amygdala (CMA), but not in the bed nucleus of the stria terminalis (BST) and the shell (AcbSh) of the nucleus accumbens (Acb) in rats treated with both morphine and naloxone. Further examination of the distribution of c-Fos-positive neurons along the rostrocaudal axis within CMA showed that the positive neurons distributed throughout this brain area and the caudal level of its central division (the central nucleus of the amygdala, CeA) exhibited the most robust labeling.
Neuronal activity can be increased by naloxone at a dose that produces conditioned place aversion 24 h after a single morphine exposure. CMA, particularly the caudal level of its central division, was of high sensitivity. The current data also suggest a possible involvement of CMA in negative motivational component of precipitated withdrawal from acute morphine dependence.</description><subject>Amygdala - metabolism</subject><subject>Analgesics, Opioid - pharmacology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Conditioning, Operant - drug effects</subject><subject>Gene Expression - drug effects</subject><subject>Genes, fos - drug effects</subject><subject>Immunohistochemistry</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Morphine</subject><subject>Morphine - pharmacology</subject><subject>Naloxone - pharmacology</subject><subject>Narcotic Antagonists - pharmacology</subject><subject>Narcotics</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Neuropharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Pharmacy</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Substance Withdrawal Syndrome - metabolism</subject><issn>0033-3158</issn><issn>1432-2072</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpdkUGLFDEQhYMo7rj6A7xIEPQWTTrVneQoi6vCghfFYyjT1TtZ0p0x6Wbdf2-GGViwLnX53qPqPcZeK_lBSWk-Vik7pYWUIJQFEPCE7RToTnTSdE_ZTkqthVa9vWAvar2TbcDCc3ahemV6C2rHll9x3Y8F7zGJuIxboJEHcZ0rp7-HQrXGvPC48HVPvODKAy1ryTONERPH-eF2xIS8A77nU04p38flliOvbSXicy6HfVzoaJbrVuglezZhqvTqvC_Zz-vPP66-ipvvX75dfboRAXq1CmNx6J0dCO0YnNU0BrCoDTgITmk3gXEDSOwdWIeDI0KjRy21GqaA5PQle3_yPZT8Z6O6-jnWQCnhQnmrvr2vtXR9A9_-B97lrSztNt8p6wwoYxqkTlAoudZCkz-UOGN58Er6YxP-1IRv-fpjEx6a5s3ZePvd4npUnKNvwLszgDVgmgouIdZHblAgBzPof5wikHQ</recordid><startdate>20041001</startdate><enddate>20041001</enddate><creator>CHUNYU JIN</creator><creator>ARAKI, Hiroaki</creator><creator>NAGATA, Mari</creator><creator>SUEMARU, Katsuya</creator><creator>SHIBATA, Kazuhiko</creator><creator>KAWASAKI, Hiromu</creator><creator>HAMAMURA, Takashi</creator><creator>GOMITA, Yutaka</creator><general>Springer</general><general>Springer Nature B.V</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>3V.</scope><scope>7QG</scope><scope>7QR</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7U7</scope><scope>C1K</scope></search><sort><creationdate>20041001</creationdate><title>Withdrawal-induced c-Fos expression in the rat centromedial amygdala 24 h following a single morphine exposure</title><author>CHUNYU JIN ; ARAKI, Hiroaki ; NAGATA, Mari ; SUEMARU, Katsuya ; SHIBATA, Kazuhiko ; KAWASAKI, Hiromu ; HAMAMURA, Takashi ; GOMITA, Yutaka</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c451t-78a65986ea8dc983edc48a37494c9139f479640a59489a69eea73d30316fcae93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Amygdala - metabolism</topic><topic>Analgesics, Opioid - pharmacology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Conditioning, Operant - drug effects</topic><topic>Gene Expression - drug effects</topic><topic>Genes, fos - drug effects</topic><topic>Immunohistochemistry</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Morphine</topic><topic>Morphine - pharmacology</topic><topic>Naloxone - pharmacology</topic><topic>Narcotic Antagonists - pharmacology</topic><topic>Narcotics</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Neuropharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Pharmacy</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Substance Withdrawal Syndrome - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>CHUNYU JIN</creatorcontrib><creatorcontrib>ARAKI, Hiroaki</creatorcontrib><creatorcontrib>NAGATA, Mari</creatorcontrib><creatorcontrib>SUEMARU, Katsuya</creatorcontrib><creatorcontrib>SHIBATA, Kazuhiko</creatorcontrib><creatorcontrib>KAWASAKI, Hiromu</creatorcontrib><creatorcontrib>HAMAMURA, Takashi</creatorcontrib><creatorcontrib>GOMITA, Yutaka</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>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Psychopharmacologia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>CHUNYU JIN</au><au>ARAKI, Hiroaki</au><au>NAGATA, Mari</au><au>SUEMARU, Katsuya</au><au>SHIBATA, Kazuhiko</au><au>KAWASAKI, Hiromu</au><au>HAMAMURA, Takashi</au><au>GOMITA, Yutaka</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Withdrawal-induced c-Fos expression in the rat centromedial amygdala 24 h following a single morphine exposure</atitle><jtitle>Psychopharmacologia</jtitle><addtitle>Psychopharmacology (Berl)</addtitle><date>2004-10-01</date><risdate>2004</risdate><volume>175</volume><issue>4</issue><spage>428</spage><epage>435</epage><pages>428-435</pages><issn>0033-3158</issn><eissn>1432-2072</eissn><coden>PSYPAG</coden><abstract>An opiate antagonist was found to induce motivational withdrawal signs 24 h or even up to 48 h after a single dose of morphine in rats.
The present study was undertaken to determine whether such a withdrawal state would modify the neuronal activity in the brain.
A conditioned place aversion was established following a one-trial paradigm in rats undergoing a single exposure to morphine (10 mg/kg) 24 h prior to naloxone administration (0.5 mg/kg). Subsequently, the expression of the protein product of c-fos gene (c-Fos) following naloxone administration was measured within the extended amygdala.
A significant increase in c-Fos immunoreactivity was seen in the centromedial amygdala (CMA), but not in the bed nucleus of the stria terminalis (BST) and the shell (AcbSh) of the nucleus accumbens (Acb) in rats treated with both morphine and naloxone. Further examination of the distribution of c-Fos-positive neurons along the rostrocaudal axis within CMA showed that the positive neurons distributed throughout this brain area and the caudal level of its central division (the central nucleus of the amygdala, CeA) exhibited the most robust labeling.
Neuronal activity can be increased by naloxone at a dose that produces conditioned place aversion 24 h after a single morphine exposure. CMA, particularly the caudal level of its central division, was of high sensitivity. The current data also suggest a possible involvement of CMA in negative motivational component of precipitated withdrawal from acute morphine dependence.</abstract><cop>Berlin</cop><pub>Springer</pub><pmid>15175841</pmid><doi>10.1007/s00213-004-1844-4</doi><tpages>8</tpages></addata></record> |
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subjects | Amygdala - metabolism Analgesics, Opioid - pharmacology Animals Biological and medical sciences Conditioning, Operant - drug effects Gene Expression - drug effects Genes, fos - drug effects Immunohistochemistry Male Medical sciences Morphine Morphine - pharmacology Naloxone - pharmacology Narcotic Antagonists - pharmacology Narcotics Neurons - drug effects Neurons - metabolism Neuropharmacology Pharmacology. Drug treatments Pharmacy Rats Rats, Sprague-Dawley Substance Withdrawal Syndrome - metabolism |
title | Withdrawal-induced c-Fos expression in the rat centromedial amygdala 24 h following a single morphine exposure |
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