Selective CRF2 receptor agonists ameliorate the anxiety- and depression-like state developed during chronic nicotine treatment and consequent acute withdrawal in mice
Abstract The aim of the present study was to investigate the effects of the selective agonists of the corticotropin-releasing factor (CRF) 2 receptor, urocortin 2 (UCN 2) and urocortin 3 (UCN 3), on the anxiety- and depression-like signs induced by acute nicotine withdrawal in mice. In order to do s...
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creator | Bagosi, Zsolt Palotai, Miklós Simon, Balázs Bokor, Péter Buzás, András Balangó, Beáta Pintér, Dávid Jászberényi, Miklós Csabafi, Krisztina Szabó, Gyula |
description | Abstract The aim of the present study was to investigate the effects of the selective agonists of the corticotropin-releasing factor (CRF) 2 receptor, urocortin 2 (UCN 2) and urocortin 3 (UCN 3), on the anxiety- and depression-like signs induced by acute nicotine withdrawal in mice. In order to do so, male CFLP mice were exposed for 7 days to repeated intraperitoneal (IP) injection with nicotine or saline solution and 1 day of acute withdrawal and then a single intracerebroventricular (ICV) injection with UCN 2, UCN 3 or saline solution. After 30 minutes the mice were observed in an elevated plus-maze test or a forced swim test, for anxiety- and depression-like behavior. After 5 minutes of testing, the plasma corticosterone concentration reflecting the activity of the hypothalamic-pituitary-adrenal (HPA) axis was also determined by a chemo-fluorescent method. Half of the animals were treated ICV and evaluated on the 8th day, the other half on the 9th day. On the 8th day, nicotine-treated mice presented signs of anxiolysis and depression, but no significant elevation of the plasma corticosterone concentration. On the 9th day, nicotine-treated mice exhibited signs of anxiety and depression and a significant increase of the plasma corticosterone levels. Central administration of UCN 2 or UCN 3 ameliorated the anxiety- and depression-like state including the hyperactivity of the HPA axis, developed during acute withdrawal following chronic nicotine treatment. The present study suggests that selective CRF2 receptor agonists could be used as a therapy in nicotine addiction. |
doi_str_mv | 10.1016/j.brainres.2016.09.044 |
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In order to do so, male CFLP mice were exposed for 7 days to repeated intraperitoneal (IP) injection with nicotine or saline solution and 1 day of acute withdrawal and then a single intracerebroventricular (ICV) injection with UCN 2, UCN 3 or saline solution. After 30 minutes the mice were observed in an elevated plus-maze test or a forced swim test, for anxiety- and depression-like behavior. After 5 minutes of testing, the plasma corticosterone concentration reflecting the activity of the hypothalamic-pituitary-adrenal (HPA) axis was also determined by a chemo-fluorescent method. Half of the animals were treated ICV and evaluated on the 8th day, the other half on the 9th day. On the 8th day, nicotine-treated mice presented signs of anxiolysis and depression, but no significant elevation of the plasma corticosterone concentration. On the 9th day, nicotine-treated mice exhibited signs of anxiety and depression and a significant increase of the plasma corticosterone levels. Central administration of UCN 2 or UCN 3 ameliorated the anxiety- and depression-like state including the hyperactivity of the HPA axis, developed during acute withdrawal following chronic nicotine treatment. The present study suggests that selective CRF2 receptor agonists could be used as a therapy in nicotine addiction.</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/j.brainres.2016.09.044</identifier><identifier>PMID: 27693397</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; Anxiety ; Anxiety - drug therapy ; Anxiety - etiology ; Anxiety - metabolism ; Corticosterone ; Corticosterone - blood ; Depression ; Depression - drug therapy ; Depression - metabolism ; Depression - pathology ; Disease Models, Animal ; Drug Evaluation, Preclinical ; Hypothalamo-Hypophyseal System - drug effects ; Hypothalamo-Hypophyseal System - metabolism ; Infusions, Intraventricular ; Male ; Mice ; Motor Activity - drug effects ; Motor Activity - physiology ; Neurology ; Nicotine ; Nicotine - pharmacology ; Nicotinic Agonists - pharmacology ; Pituitary-Adrenal System - drug effects ; Pituitary-Adrenal System - metabolism ; Psychotropic Drugs - administration & dosage ; Receptors, Corticotropin-Releasing Hormone - agonists ; Receptors, Corticotropin-Releasing Hormone - metabolism ; Substance Withdrawal Syndrome - drug therapy ; Substance Withdrawal Syndrome - metabolism ; Substance Withdrawal Syndrome - psychology ; Tobacco Use Disorder - drug therapy ; Tobacco Use Disorder - metabolism ; Tobacco Use Disorder - psychology ; Urocortin ; Urocortins - administration & dosage</subject><ispartof>Brain research, 2016-12, Vol.1652, p.21-29</ispartof><rights>Elsevier B.V.</rights><rights>2016 Elsevier B.V.</rights><rights>Copyright © 2016 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c456t-cae8b7648c65cf23a3db9f97db092e387f9a1767a76649ef2e7d30b830b6885f3</citedby><cites>FETCH-LOGICAL-c456t-cae8b7648c65cf23a3db9f97db092e387f9a1767a76649ef2e7d30b830b6885f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0006899316306916$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27693397$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bagosi, Zsolt</creatorcontrib><creatorcontrib>Palotai, Miklós</creatorcontrib><creatorcontrib>Simon, Balázs</creatorcontrib><creatorcontrib>Bokor, Péter</creatorcontrib><creatorcontrib>Buzás, András</creatorcontrib><creatorcontrib>Balangó, Beáta</creatorcontrib><creatorcontrib>Pintér, Dávid</creatorcontrib><creatorcontrib>Jászberényi, Miklós</creatorcontrib><creatorcontrib>Csabafi, Krisztina</creatorcontrib><creatorcontrib>Szabó, Gyula</creatorcontrib><title>Selective CRF2 receptor agonists ameliorate the anxiety- and depression-like state developed during chronic nicotine treatment and consequent acute withdrawal in mice</title><title>Brain research</title><addtitle>Brain Res</addtitle><description>Abstract The aim of the present study was to investigate the effects of the selective agonists of the corticotropin-releasing factor (CRF) 2 receptor, urocortin 2 (UCN 2) and urocortin 3 (UCN 3), on the anxiety- and depression-like signs induced by acute nicotine withdrawal in mice. In order to do so, male CFLP mice were exposed for 7 days to repeated intraperitoneal (IP) injection with nicotine or saline solution and 1 day of acute withdrawal and then a single intracerebroventricular (ICV) injection with UCN 2, UCN 3 or saline solution. After 30 minutes the mice were observed in an elevated plus-maze test or a forced swim test, for anxiety- and depression-like behavior. After 5 minutes of testing, the plasma corticosterone concentration reflecting the activity of the hypothalamic-pituitary-adrenal (HPA) axis was also determined by a chemo-fluorescent method. Half of the animals were treated ICV and evaluated on the 8th day, the other half on the 9th day. On the 8th day, nicotine-treated mice presented signs of anxiolysis and depression, but no significant elevation of the plasma corticosterone concentration. On the 9th day, nicotine-treated mice exhibited signs of anxiety and depression and a significant increase of the plasma corticosterone levels. Central administration of UCN 2 or UCN 3 ameliorated the anxiety- and depression-like state including the hyperactivity of the HPA axis, developed during acute withdrawal following chronic nicotine treatment. The present study suggests that selective CRF2 receptor agonists could be used as a therapy in nicotine addiction.</description><subject>Animals</subject><subject>Anxiety</subject><subject>Anxiety - drug therapy</subject><subject>Anxiety - etiology</subject><subject>Anxiety - metabolism</subject><subject>Corticosterone</subject><subject>Corticosterone - blood</subject><subject>Depression</subject><subject>Depression - drug therapy</subject><subject>Depression - metabolism</subject><subject>Depression - pathology</subject><subject>Disease Models, Animal</subject><subject>Drug Evaluation, Preclinical</subject><subject>Hypothalamo-Hypophyseal System - drug effects</subject><subject>Hypothalamo-Hypophyseal System - metabolism</subject><subject>Infusions, Intraventricular</subject><subject>Male</subject><subject>Mice</subject><subject>Motor Activity - drug effects</subject><subject>Motor Activity - physiology</subject><subject>Neurology</subject><subject>Nicotine</subject><subject>Nicotine - pharmacology</subject><subject>Nicotinic Agonists - pharmacology</subject><subject>Pituitary-Adrenal System - drug effects</subject><subject>Pituitary-Adrenal System - metabolism</subject><subject>Psychotropic Drugs - administration & dosage</subject><subject>Receptors, Corticotropin-Releasing Hormone - agonists</subject><subject>Receptors, Corticotropin-Releasing Hormone - metabolism</subject><subject>Substance Withdrawal Syndrome - drug therapy</subject><subject>Substance Withdrawal Syndrome - metabolism</subject><subject>Substance Withdrawal Syndrome - psychology</subject><subject>Tobacco Use Disorder - drug therapy</subject><subject>Tobacco Use Disorder - metabolism</subject><subject>Tobacco Use Disorder - psychology</subject><subject>Urocortin</subject><subject>Urocortins - administration & dosage</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNUsFu1DAQjRCILoVfqHzkksWJHTu-INCKAlIlJApny3EmXW8TO9jOlv0hvpPZbsuBCxxmPCO_eTOaN0VxUdF1RSvxZrfuonE-QlrXmK-pWlPOnxSrqpV1KWpOnxYrSqkoW6XYWfEipR2mjCn6vDirpVAYylXx6xpGsNntgWy-XtYkgoU5h0jMTfAu5UTMBKML0WQgeQvE-J8O8qHEoCc9zDhBcsGXo7sFkvIR1sMexjAD_i_R-RtitxHJLEEL2XkkimDyBD7fs9jgE_xY7lO7IMGdy9s-mjszEufJ5Cy8LJ4NZkzw6uE9L75ffvi2-VReffn4efP-qrS8Ebm0BtpOCt5a0dihZob1nRqU7DuqamCtHJSppJBGCsEVDDXIntGuRRNt2wzsvHh94p1jwIlS1pNLFsbReAhL0lXLBaeSV_w_oKxhvG1qhlBxgtoYUoow6Dm6ycSDrqg-yql3-lFOfZRTU6VRTiy8eOixdBP0f8oe9UPAuxMAcCl7B1En68Bb6B0qmXUf3L97vP2Lwo4OlTLjLRwg7cISPa5cVzrVmurr41Edb6oSjAqF_jc-CM1c</recordid><startdate>20161201</startdate><enddate>20161201</enddate><creator>Bagosi, Zsolt</creator><creator>Palotai, Miklós</creator><creator>Simon, Balázs</creator><creator>Bokor, Péter</creator><creator>Buzás, András</creator><creator>Balangó, Beáta</creator><creator>Pintér, Dávid</creator><creator>Jászberényi, Miklós</creator><creator>Csabafi, Krisztina</creator><creator>Szabó, Gyula</creator><general>Elsevier B.V</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>7X8</scope><scope>7QG</scope><scope>7TK</scope></search><sort><creationdate>20161201</creationdate><title>Selective CRF2 receptor agonists ameliorate the anxiety- and depression-like state developed during chronic nicotine treatment and consequent acute withdrawal in mice</title><author>Bagosi, Zsolt ; Palotai, Miklós ; Simon, Balázs ; Bokor, Péter ; Buzás, András ; Balangó, Beáta ; Pintér, Dávid ; Jászberényi, Miklós ; Csabafi, Krisztina ; Szabó, Gyula</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c456t-cae8b7648c65cf23a3db9f97db092e387f9a1767a76649ef2e7d30b830b6885f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Anxiety</topic><topic>Anxiety - drug therapy</topic><topic>Anxiety - etiology</topic><topic>Anxiety - metabolism</topic><topic>Corticosterone</topic><topic>Corticosterone - blood</topic><topic>Depression</topic><topic>Depression - drug therapy</topic><topic>Depression - metabolism</topic><topic>Depression - pathology</topic><topic>Disease Models, Animal</topic><topic>Drug Evaluation, Preclinical</topic><topic>Hypothalamo-Hypophyseal System - drug effects</topic><topic>Hypothalamo-Hypophyseal System - metabolism</topic><topic>Infusions, Intraventricular</topic><topic>Male</topic><topic>Mice</topic><topic>Motor Activity - drug effects</topic><topic>Motor Activity - physiology</topic><topic>Neurology</topic><topic>Nicotine</topic><topic>Nicotine - pharmacology</topic><topic>Nicotinic Agonists - pharmacology</topic><topic>Pituitary-Adrenal System - drug effects</topic><topic>Pituitary-Adrenal System - metabolism</topic><topic>Psychotropic Drugs - administration & dosage</topic><topic>Receptors, Corticotropin-Releasing Hormone - agonists</topic><topic>Receptors, Corticotropin-Releasing Hormone - metabolism</topic><topic>Substance Withdrawal Syndrome - drug therapy</topic><topic>Substance Withdrawal Syndrome - metabolism</topic><topic>Substance Withdrawal Syndrome - psychology</topic><topic>Tobacco Use Disorder - drug therapy</topic><topic>Tobacco Use Disorder - metabolism</topic><topic>Tobacco Use Disorder - psychology</topic><topic>Urocortin</topic><topic>Urocortins - administration & dosage</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bagosi, Zsolt</creatorcontrib><creatorcontrib>Palotai, Miklós</creatorcontrib><creatorcontrib>Simon, Balázs</creatorcontrib><creatorcontrib>Bokor, Péter</creatorcontrib><creatorcontrib>Buzás, András</creatorcontrib><creatorcontrib>Balangó, Beáta</creatorcontrib><creatorcontrib>Pintér, Dávid</creatorcontrib><creatorcontrib>Jászberényi, Miklós</creatorcontrib><creatorcontrib>Csabafi, Krisztina</creatorcontrib><creatorcontrib>Szabó, Gyula</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Animal Behavior Abstracts</collection><collection>Neurosciences Abstracts</collection><jtitle>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bagosi, Zsolt</au><au>Palotai, Miklós</au><au>Simon, Balázs</au><au>Bokor, Péter</au><au>Buzás, András</au><au>Balangó, Beáta</au><au>Pintér, Dávid</au><au>Jászberényi, Miklós</au><au>Csabafi, Krisztina</au><au>Szabó, Gyula</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Selective CRF2 receptor agonists ameliorate the anxiety- and depression-like state developed during chronic nicotine treatment and consequent acute withdrawal in mice</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>2016-12-01</date><risdate>2016</risdate><volume>1652</volume><spage>21</spage><epage>29</epage><pages>21-29</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><abstract>Abstract The aim of the present study was to investigate the effects of the selective agonists of the corticotropin-releasing factor (CRF) 2 receptor, urocortin 2 (UCN 2) and urocortin 3 (UCN 3), on the anxiety- and depression-like signs induced by acute nicotine withdrawal in mice. In order to do so, male CFLP mice were exposed for 7 days to repeated intraperitoneal (IP) injection with nicotine or saline solution and 1 day of acute withdrawal and then a single intracerebroventricular (ICV) injection with UCN 2, UCN 3 or saline solution. After 30 minutes the mice were observed in an elevated plus-maze test or a forced swim test, for anxiety- and depression-like behavior. After 5 minutes of testing, the plasma corticosterone concentration reflecting the activity of the hypothalamic-pituitary-adrenal (HPA) axis was also determined by a chemo-fluorescent method. Half of the animals were treated ICV and evaluated on the 8th day, the other half on the 9th day. On the 8th day, nicotine-treated mice presented signs of anxiolysis and depression, but no significant elevation of the plasma corticosterone concentration. On the 9th day, nicotine-treated mice exhibited signs of anxiety and depression and a significant increase of the plasma corticosterone levels. Central administration of UCN 2 or UCN 3 ameliorated the anxiety- and depression-like state including the hyperactivity of the HPA axis, developed during acute withdrawal following chronic nicotine treatment. The present study suggests that selective CRF2 receptor agonists could be used as a therapy in nicotine addiction.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>27693397</pmid><doi>10.1016/j.brainres.2016.09.044</doi><tpages>9</tpages></addata></record> |
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subjects | Animals Anxiety Anxiety - drug therapy Anxiety - etiology Anxiety - metabolism Corticosterone Corticosterone - blood Depression Depression - drug therapy Depression - metabolism Depression - pathology Disease Models, Animal Drug Evaluation, Preclinical Hypothalamo-Hypophyseal System - drug effects Hypothalamo-Hypophyseal System - metabolism Infusions, Intraventricular Male Mice Motor Activity - drug effects Motor Activity - physiology Neurology Nicotine Nicotine - pharmacology Nicotinic Agonists - pharmacology Pituitary-Adrenal System - drug effects Pituitary-Adrenal System - metabolism Psychotropic Drugs - administration & dosage Receptors, Corticotropin-Releasing Hormone - agonists Receptors, Corticotropin-Releasing Hormone - metabolism Substance Withdrawal Syndrome - drug therapy Substance Withdrawal Syndrome - metabolism Substance Withdrawal Syndrome - psychology Tobacco Use Disorder - drug therapy Tobacco Use Disorder - metabolism Tobacco Use Disorder - psychology Urocortin Urocortins - administration & dosage |
title | Selective CRF2 receptor agonists ameliorate the anxiety- and depression-like state developed during chronic nicotine treatment and consequent acute withdrawal in mice |
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