Repeated social defeat-induced depression-like behavioral and biological alterations in rats: involvement of cholecystokinin
Cholecystokinin (CCK) involvement in depression-like disorders is poorly documented. Here, we investigated whether CCKergic neurotransmission is relevant to depressive-like symptoms and antidepressant therapy using a novel preclinical model based on repeated social defeat over 4 weeks in rats. Repea...
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description | Cholecystokinin (CCK) involvement in depression-like disorders is poorly documented. Here, we investigated whether CCKergic neurotransmission is relevant to depressive-like symptoms and antidepressant therapy using a novel preclinical model based on repeated social defeat over 4 weeks in rats. Repeated social defeat triggers changes that could be considered as behavioral and biological correlates of depressive symptoms in humans, such as a hyperactivity of hypothalamic–pituitary–adrenal (HPA) axis (increase of serum corticosterone levels and of adrenal gland weight), increased immobility time in the forced swimming test (FST), decrease of body weight and of sweet water consumption and reduction of hippocampal volume associated with a decreased cell proliferation in the dentate gyrus. In addition,
in vivo
microdialysis showed that cortical CCK release was tonically increased in defeated rats. Chronic imipramine treatment (16 mg kg
−1
per day for 25 days) prevented both the repeated social defeat-induced alterations of biological and behavioral parameters and the associated increase of cortical CCK release. Chronic blockade of CCK2 receptors by the specific antagonist CI-988 (1 mg kg
−1
per day for 25 days) also normalized immobility time in the FST and prevented HPA axis hyperactivity, reduction of hippocampal volume and cell proliferation and decreased sweet water intake normally evoked by repeated social defeat. These data showed that the repeated social-defeat paradigm can be considered as a suitable model of ‘depression’ in rats. The causal link between social defeat-evoked (1) increase in cortical CCKergic neurotransmission and (2) depression-like symptoms that we highlighted here strongly suggests that CCKergic systems may be a relevant target for novel antidepressant therapy. |
doi_str_mv | 10.1038/sj.mp.4002097 |
format | Article |
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in vivo
microdialysis showed that cortical CCK release was tonically increased in defeated rats. Chronic imipramine treatment (16 mg kg
−1
per day for 25 days) prevented both the repeated social defeat-induced alterations of biological and behavioral parameters and the associated increase of cortical CCK release. Chronic blockade of CCK2 receptors by the specific antagonist CI-988 (1 mg kg
−1
per day for 25 days) also normalized immobility time in the FST and prevented HPA axis hyperactivity, reduction of hippocampal volume and cell proliferation and decreased sweet water intake normally evoked by repeated social defeat. These data showed that the repeated social-defeat paradigm can be considered as a suitable model of ‘depression’ in rats. The causal link between social defeat-evoked (1) increase in cortical CCKergic neurotransmission and (2) depression-like symptoms that we highlighted here strongly suggests that CCKergic systems may be a relevant target for novel antidepressant therapy.</description><identifier>ISSN: 1359-4184</identifier><identifier>EISSN: 1476-5578</identifier><identifier>DOI: 10.1038/sj.mp.4002097</identifier><identifier>PMID: 17893702</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Adrenal glands ; Adult and adolescent clinical studies ; Analysis of Variance ; Animals ; Antidepressants ; Antidepressive Agents, Tricyclic - therapeutic use ; Anxiety ; Behavioral Sciences ; Biological and medical sciences ; Biological Psychology ; Body weight ; Bromodeoxyuridine - metabolism ; Cell growth ; Cell Proliferation ; Cholecystokinin ; Cholecystokinin - metabolism ; Corticosterone ; Corticosterone - blood ; Dentate gyrus ; Depression ; Depression - drug therapy ; Depression - etiology ; Depression - metabolism ; Depression - pathology ; Depression, Mental ; Disease Models, Animal ; Dominance-Subordination ; Dosage and administration ; Drug therapy ; Gene Expression Regulation - physiology ; Genetic aspects ; Glial Fibrillary Acidic Protein - metabolism ; Health aspects ; Hippocampus ; Hippocampus - physiopathology ; Hyperactivity ; Hypothalamic-pituitary-adrenal axis ; Hypothalamus ; Imipramine ; Imipramine - therapeutic use ; Male ; Medical sciences ; Medicine ; Medicine & Public Health ; Mental depression ; Microdialysis ; Microdialysis - methods ; Mood disorders ; Neuropharmacology ; Neurosciences ; Neurotransmission ; original-article ; Pharmacology. Drug treatments ; Pharmacotherapy ; Phosphopyruvate Hydratase - metabolism ; Pituitary ; Psychiatry ; Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer ; Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease) ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; Psychopharmacology ; Radioimmunoassay - methods ; Rats ; Rats, Sprague-Dawley ; Social Environment ; Social interactions ; Stress ; Swimming ; Validation studies ; Validity ; Water intake</subject><ispartof>Molecular psychiatry, 2008-12, Vol.13 (12), p.1079-1092</ispartof><rights>Springer Nature Limited 2008</rights><rights>2009 INIST-CNRS</rights><rights>COPYRIGHT 2008 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Dec 2008</rights><rights>Nature Publishing Group 2008.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c650t-a9af2852713b6779dafd26a5a2693690dc23754fcf648d38006dc6547d5cacec3</citedby><cites>FETCH-LOGICAL-c650t-a9af2852713b6779dafd26a5a2693690dc23754fcf648d38006dc6547d5cacec3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/sj.mp.4002097$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/sj.mp.4002097$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20841978$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17893702$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Becker, C</creatorcontrib><creatorcontrib>Zeau, B</creatorcontrib><creatorcontrib>Rivat, C</creatorcontrib><creatorcontrib>Blugeot, A</creatorcontrib><creatorcontrib>Hamon, M</creatorcontrib><creatorcontrib>Benoliel, J-J</creatorcontrib><title>Repeated social defeat-induced depression-like behavioral and biological alterations in rats: involvement of cholecystokinin</title><title>Molecular psychiatry</title><addtitle>Mol Psychiatry</addtitle><addtitle>Mol Psychiatry</addtitle><description>Cholecystokinin (CCK) involvement in depression-like disorders is poorly documented. Here, we investigated whether CCKergic neurotransmission is relevant to depressive-like symptoms and antidepressant therapy using a novel preclinical model based on repeated social defeat over 4 weeks in rats. Repeated social defeat triggers changes that could be considered as behavioral and biological correlates of depressive symptoms in humans, such as a hyperactivity of hypothalamic–pituitary–adrenal (HPA) axis (increase of serum corticosterone levels and of adrenal gland weight), increased immobility time in the forced swimming test (FST), decrease of body weight and of sweet water consumption and reduction of hippocampal volume associated with a decreased cell proliferation in the dentate gyrus. In addition,
in vivo
microdialysis showed that cortical CCK release was tonically increased in defeated rats. Chronic imipramine treatment (16 mg kg
−1
per day for 25 days) prevented both the repeated social defeat-induced alterations of biological and behavioral parameters and the associated increase of cortical CCK release. Chronic blockade of CCK2 receptors by the specific antagonist CI-988 (1 mg kg
−1
per day for 25 days) also normalized immobility time in the FST and prevented HPA axis hyperactivity, reduction of hippocampal volume and cell proliferation and decreased sweet water intake normally evoked by repeated social defeat. These data showed that the repeated social-defeat paradigm can be considered as a suitable model of ‘depression’ in rats. The causal link between social defeat-evoked (1) increase in cortical CCKergic neurotransmission and (2) depression-like symptoms that we highlighted here strongly suggests that CCKergic systems may be a relevant target for novel antidepressant therapy.</description><subject>Adrenal glands</subject><subject>Adult and adolescent clinical studies</subject><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Antidepressants</subject><subject>Antidepressive Agents, Tricyclic - therapeutic use</subject><subject>Anxiety</subject><subject>Behavioral Sciences</subject><subject>Biological and medical sciences</subject><subject>Biological Psychology</subject><subject>Body weight</subject><subject>Bromodeoxyuridine - metabolism</subject><subject>Cell growth</subject><subject>Cell Proliferation</subject><subject>Cholecystokinin</subject><subject>Cholecystokinin - metabolism</subject><subject>Corticosterone</subject><subject>Corticosterone - blood</subject><subject>Dentate gyrus</subject><subject>Depression</subject><subject>Depression - drug therapy</subject><subject>Depression - etiology</subject><subject>Depression - metabolism</subject><subject>Depression - pathology</subject><subject>Depression, Mental</subject><subject>Disease Models, Animal</subject><subject>Dominance-Subordination</subject><subject>Dosage and administration</subject><subject>Drug therapy</subject><subject>Gene Expression Regulation - physiology</subject><subject>Genetic aspects</subject><subject>Glial Fibrillary Acidic Protein - metabolism</subject><subject>Health aspects</subject><subject>Hippocampus</subject><subject>Hippocampus - physiopathology</subject><subject>Hyperactivity</subject><subject>Hypothalamic-pituitary-adrenal axis</subject><subject>Hypothalamus</subject><subject>Imipramine</subject><subject>Imipramine - therapeutic use</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mental depression</subject><subject>Microdialysis</subject><subject>Microdialysis - methods</subject><subject>Mood disorders</subject><subject>Neuropharmacology</subject><subject>Neurosciences</subject><subject>Neurotransmission</subject><subject>original-article</subject><subject>Pharmacology. Drug treatments</subject><subject>Pharmacotherapy</subject><subject>Phosphopyruvate Hydratase - metabolism</subject><subject>Pituitary</subject><subject>Psychiatry</subject><subject>Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer</subject><subject>Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease)</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. Psychiatry</subject><subject>Psychopharmacology</subject><subject>Radioimmunoassay - methods</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Social Environment</subject><subject>Social interactions</subject><subject>Stress</subject><subject>Swimming</subject><subject>Validation studies</subject><subject>Validity</subject><subject>Water intake</subject><issn>1359-4184</issn><issn>1476-5578</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkttrFDEUhwdRbK0--iqDoj7Nmvulb6V4g4Ig-jxkk5M225lkTGYXCv7xZujiqlQlDznn5PudSzhN8xSjFUZUvSmb1TitGEIEaXmvOcZMio5zqe5Xm3LdMazYUfOolA1CyyN_2BxhqTSViBw33z_DBGYG15ZkgxlaB776XYhua2vUwZShlJBiN4RraNdwZXYh5Uqa6Np1SEO6DHZxhxmymStZ2hDbapbTauzSsIMR4twm39qrNIC9KXO6DjHEx80Db4YCT_b3SfP13dsv5x-6i0_vP56fXXRWcDR3RhtPFCcS07WQUjvjHRGGGyI0FRo5S6jkzFsvmHJUISRcVTLpuDUWLD1pXt_mnXL6toUy92MoFobBREjb0kuuKeZVXMlX_ySFlopjhv4LYs2RVpJW8MUf4CZtc6zj9kQwLgUTeKn7_K8UwYQyqn5JdWkG6EP0ac7GLnX7M6wRUQKzhVrdQdXjYAw2RfChxn8TdLcCm1MpGXw_5TCafNNj1C871pdNP079fscq_2zf63Y9gjvQ-6WqwMs9YErdDJ9NtKH85AhSDNd_PHRa6lO8hHwY-u7KPwAw7OiA</recordid><startdate>20081201</startdate><enddate>20081201</enddate><creator>Becker, C</creator><creator>Zeau, B</creator><creator>Rivat, C</creator><creator>Blugeot, A</creator><creator>Hamon, M</creator><creator>Benoliel, J-J</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20081201</creationdate><title>Repeated social defeat-induced depression-like behavioral and biological alterations in rats: involvement of cholecystokinin</title><author>Becker, C ; Zeau, B ; Rivat, C ; Blugeot, A ; Hamon, M ; Benoliel, J-J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c650t-a9af2852713b6779dafd26a5a2693690dc23754fcf648d38006dc6547d5cacec3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adrenal glands</topic><topic>Adult and adolescent clinical studies</topic><topic>Analysis of Variance</topic><topic>Animals</topic><topic>Antidepressants</topic><topic>Antidepressive Agents, Tricyclic - therapeutic use</topic><topic>Anxiety</topic><topic>Behavioral Sciences</topic><topic>Biological and medical sciences</topic><topic>Biological Psychology</topic><topic>Body weight</topic><topic>Bromodeoxyuridine - metabolism</topic><topic>Cell growth</topic><topic>Cell Proliferation</topic><topic>Cholecystokinin</topic><topic>Cholecystokinin - metabolism</topic><topic>Corticosterone</topic><topic>Corticosterone - blood</topic><topic>Dentate gyrus</topic><topic>Depression</topic><topic>Depression - drug therapy</topic><topic>Depression - etiology</topic><topic>Depression - metabolism</topic><topic>Depression - pathology</topic><topic>Depression, Mental</topic><topic>Disease Models, Animal</topic><topic>Dominance-Subordination</topic><topic>Dosage and administration</topic><topic>Drug therapy</topic><topic>Gene Expression Regulation - physiology</topic><topic>Genetic aspects</topic><topic>Glial Fibrillary Acidic Protein - metabolism</topic><topic>Health aspects</topic><topic>Hippocampus</topic><topic>Hippocampus - physiopathology</topic><topic>Hyperactivity</topic><topic>Hypothalamic-pituitary-adrenal axis</topic><topic>Hypothalamus</topic><topic>Imipramine</topic><topic>Imipramine - therapeutic use</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mental depression</topic><topic>Microdialysis</topic><topic>Microdialysis - methods</topic><topic>Mood disorders</topic><topic>Neuropharmacology</topic><topic>Neurosciences</topic><topic>Neurotransmission</topic><topic>original-article</topic><topic>Pharmacology. Drug treatments</topic><topic>Pharmacotherapy</topic><topic>Phosphopyruvate Hydratase - metabolism</topic><topic>Pituitary</topic><topic>Psychiatry</topic><topic>Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer</topic><topic>Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease)</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopathology. Psychiatry</topic><topic>Psychopharmacology</topic><topic>Radioimmunoassay - methods</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Social Environment</topic><topic>Social interactions</topic><topic>Stress</topic><topic>Swimming</topic><topic>Validation studies</topic><topic>Validity</topic><topic>Water intake</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Becker, C</creatorcontrib><creatorcontrib>Zeau, B</creatorcontrib><creatorcontrib>Rivat, C</creatorcontrib><creatorcontrib>Blugeot, A</creatorcontrib><creatorcontrib>Hamon, M</creatorcontrib><creatorcontrib>Benoliel, J-J</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>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>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Psychology</collection><collection>Biological Science Database</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>MEDLINE - Academic</collection><jtitle>Molecular psychiatry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Becker, C</au><au>Zeau, B</au><au>Rivat, C</au><au>Blugeot, A</au><au>Hamon, M</au><au>Benoliel, J-J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Repeated social defeat-induced depression-like behavioral and biological alterations in rats: involvement of cholecystokinin</atitle><jtitle>Molecular psychiatry</jtitle><stitle>Mol Psychiatry</stitle><addtitle>Mol Psychiatry</addtitle><date>2008-12-01</date><risdate>2008</risdate><volume>13</volume><issue>12</issue><spage>1079</spage><epage>1092</epage><pages>1079-1092</pages><issn>1359-4184</issn><eissn>1476-5578</eissn><abstract>Cholecystokinin (CCK) involvement in depression-like disorders is poorly documented. Here, we investigated whether CCKergic neurotransmission is relevant to depressive-like symptoms and antidepressant therapy using a novel preclinical model based on repeated social defeat over 4 weeks in rats. Repeated social defeat triggers changes that could be considered as behavioral and biological correlates of depressive symptoms in humans, such as a hyperactivity of hypothalamic–pituitary–adrenal (HPA) axis (increase of serum corticosterone levels and of adrenal gland weight), increased immobility time in the forced swimming test (FST), decrease of body weight and of sweet water consumption and reduction of hippocampal volume associated with a decreased cell proliferation in the dentate gyrus. In addition,
in vivo
microdialysis showed that cortical CCK release was tonically increased in defeated rats. Chronic imipramine treatment (16 mg kg
−1
per day for 25 days) prevented both the repeated social defeat-induced alterations of biological and behavioral parameters and the associated increase of cortical CCK release. Chronic blockade of CCK2 receptors by the specific antagonist CI-988 (1 mg kg
−1
per day for 25 days) also normalized immobility time in the FST and prevented HPA axis hyperactivity, reduction of hippocampal volume and cell proliferation and decreased sweet water intake normally evoked by repeated social defeat. These data showed that the repeated social-defeat paradigm can be considered as a suitable model of ‘depression’ in rats. The causal link between social defeat-evoked (1) increase in cortical CCKergic neurotransmission and (2) depression-like symptoms that we highlighted here strongly suggests that CCKergic systems may be a relevant target for novel antidepressant therapy.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>17893702</pmid><doi>10.1038/sj.mp.4002097</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adrenal glands Adult and adolescent clinical studies Analysis of Variance Animals Antidepressants Antidepressive Agents, Tricyclic - therapeutic use Anxiety Behavioral Sciences Biological and medical sciences Biological Psychology Body weight Bromodeoxyuridine - metabolism Cell growth Cell Proliferation Cholecystokinin Cholecystokinin - metabolism Corticosterone Corticosterone - blood Dentate gyrus Depression Depression - drug therapy Depression - etiology Depression - metabolism Depression - pathology Depression, Mental Disease Models, Animal Dominance-Subordination Dosage and administration Drug therapy Gene Expression Regulation - physiology Genetic aspects Glial Fibrillary Acidic Protein - metabolism Health aspects Hippocampus Hippocampus - physiopathology Hyperactivity Hypothalamic-pituitary-adrenal axis Hypothalamus Imipramine Imipramine - therapeutic use Male Medical sciences Medicine Medicine & Public Health Mental depression Microdialysis Microdialysis - methods Mood disorders Neuropharmacology Neurosciences Neurotransmission original-article Pharmacology. Drug treatments Pharmacotherapy Phosphopyruvate Hydratase - metabolism Pituitary Psychiatry Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease) Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Psychopharmacology Radioimmunoassay - methods Rats Rats, Sprague-Dawley Social Environment Social interactions Stress Swimming Validation studies Validity Water intake |
title | Repeated social defeat-induced depression-like behavioral and biological alterations in rats: involvement of cholecystokinin |
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