Effects of postnatal anoxia on striatal dopamine metabolism and prepulse inhibition in rats
Various evidence indicate that schizophrenia is a neurodevelopmental disorder. Epidemiological observations point to oxygen deficiencies during delivery as one of the early risk factors for developing schizophrenia. The aim of the present study was to examine the effect of postnatal anoxia in rats....
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| Veröffentlicht in: | Pharmacology, biochemistry and behavior biochemistry and behavior, 2004-04, Vol.77 (4), p.767-774 |
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| creator | Sandager-Nielsen, Karin Andersen, Maibritt B Sager, Thomas N Werge, Thomas Scheel-Krüger, Jørgen |
| description | Various evidence indicate that schizophrenia is a neurodevelopmental disorder. Epidemiological observations point to oxygen deficiencies during delivery as one of the early risk factors for developing schizophrenia. The aim of the present study was to examine the effect of postnatal anoxia in rats. Anoxia was experimentally induced by placing 9-day-old rat pups for 6 min in a chamber saturated with 100% nitrogen (N
2). Exposure to anoxia on postnatal day (PND) 9 resulted in significantly reduced subcortical dopamine metabolism and turnover, as measured by striatal 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) concentrations. Furthermore, in the anoxic group only, striatal HVA concentrations were negatively correlated to prefrontal cortical
N-acetylaspartate (NAA) levels. Similar findings of distorted prefrontal–subcortical interactions have recently been reported in schizophrenic patients. There was no effect of postnatal anoxia on either baseline or
d-amphetamine-induced deficit in the prepulse inhibition (PPI) paradigm in adulthood. Accordingly, although oxygen deficiency early in life has been discussed as vulnerability factor in developing schizophrenia, exposure to postnatal anoxia in the rat does not show clear-cut phenomenological similarities with the disorder. |
| doi_str_mv | 10.1016/j.pbb.2004.01.017 |
| format | Article |
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2). Exposure to anoxia on postnatal day (PND) 9 resulted in significantly reduced subcortical dopamine metabolism and turnover, as measured by striatal 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) concentrations. Furthermore, in the anoxic group only, striatal HVA concentrations were negatively correlated to prefrontal cortical
N-acetylaspartate (NAA) levels. Similar findings of distorted prefrontal–subcortical interactions have recently been reported in schizophrenic patients. There was no effect of postnatal anoxia on either baseline or
d-amphetamine-induced deficit in the prepulse inhibition (PPI) paradigm in adulthood. Accordingly, although oxygen deficiency early in life has been discussed as vulnerability factor in developing schizophrenia, exposure to postnatal anoxia in the rat does not show clear-cut phenomenological similarities with the disorder.</description><identifier>ISSN: 0091-3057</identifier><identifier>EISSN: 1873-5177</identifier><identifier>DOI: 10.1016/j.pbb.2004.01.017</identifier><identifier>PMID: 15099922</identifier><identifier>CODEN: PBBHAU</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Age Factors ; Animal model ; Animals ; Animals, Newborn ; Anoxia ; Biological and medical sciences ; Corpus Striatum - metabolism ; Dopamine ; Dopamine - metabolism ; Female ; Fundamental and applied biological sciences. Psychology ; Hypoxia, Brain - metabolism ; Male ; Medical sciences ; N-acetylaspartate ; Neuropharmacology ; Pharmacology. Drug treatments ; Prepulse inhibition ; Psychology. Psychoanalysis. Psychiatry ; Psychology. Psychophysiology ; Rats ; Rats, Wistar ; Reflex, Startle - physiology ; Schizophrenia</subject><ispartof>Pharmacology, biochemistry and behavior, 2004-04, Vol.77 (4), p.767-774</ispartof><rights>2004 Elsevier Inc.</rights><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c476t-5a7cb60b421f992f5f2d10af0ae4c96a00a17e3b90940b62c34218b662465ab83</citedby><cites>FETCH-LOGICAL-c476t-5a7cb60b421f992f5f2d10af0ae4c96a00a17e3b90940b62c34218b662465ab83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0091305704000334$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15678247$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15099922$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sandager-Nielsen, Karin</creatorcontrib><creatorcontrib>Andersen, Maibritt B</creatorcontrib><creatorcontrib>Sager, Thomas N</creatorcontrib><creatorcontrib>Werge, Thomas</creatorcontrib><creatorcontrib>Scheel-Krüger, Jørgen</creatorcontrib><title>Effects of postnatal anoxia on striatal dopamine metabolism and prepulse inhibition in rats</title><title>Pharmacology, biochemistry and behavior</title><addtitle>Pharmacol Biochem Behav</addtitle><description>Various evidence indicate that schizophrenia is a neurodevelopmental disorder. Epidemiological observations point to oxygen deficiencies during delivery as one of the early risk factors for developing schizophrenia. The aim of the present study was to examine the effect of postnatal anoxia in rats. Anoxia was experimentally induced by placing 9-day-old rat pups for 6 min in a chamber saturated with 100% nitrogen (N
2). Exposure to anoxia on postnatal day (PND) 9 resulted in significantly reduced subcortical dopamine metabolism and turnover, as measured by striatal 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) concentrations. Furthermore, in the anoxic group only, striatal HVA concentrations were negatively correlated to prefrontal cortical
N-acetylaspartate (NAA) levels. Similar findings of distorted prefrontal–subcortical interactions have recently been reported in schizophrenic patients. There was no effect of postnatal anoxia on either baseline or
d-amphetamine-induced deficit in the prepulse inhibition (PPI) paradigm in adulthood. Accordingly, although oxygen deficiency early in life has been discussed as vulnerability factor in developing schizophrenia, exposure to postnatal anoxia in the rat does not show clear-cut phenomenological similarities with the disorder.</description><subject>Age Factors</subject><subject>Animal model</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Anoxia</subject><subject>Biological and medical sciences</subject><subject>Corpus Striatum - metabolism</subject><subject>Dopamine</subject><subject>Dopamine - metabolism</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hypoxia, Brain - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>N-acetylaspartate</subject><subject>Neuropharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Prepulse inhibition</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychology. Psychophysiology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reflex, Startle - physiology</subject><subject>Schizophrenia</subject><issn>0091-3057</issn><issn>1873-5177</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc2KFDEURoMoTjv6AG4kG91Ve5OqSiq4kmH8gQE3unIRblIJpqlKyiQtztubtht0pXAhkJzv43JCyHMGewZMvD7sN2P2HGDYA2sjH5Adm2TfjUzKh2QHoFjXwyivyJNSDtBALuRjcsVGUEpxviNfb713thaaPN1SqRErLhRj-hmQpkhLzeH31Zw2XEN0dHUVTVpCWRs20y277bgUR0P8FkyooYVCpBlreUoeeWxPzy7nNfny7vbzzYfu7tP7jzdv7zo7SFG7EaU1AszAmW9L-dHzmQF6QDdYJRAAmXS9UaAGMILbvpGTEYIPYkQz9dfk1bl3y-n70ZWq11CsWxaMLh2LlmwaR66G_4JMqtbNRQPZGbQ5lZKd11sOK-Z7zUCf1OuDbur1Sb0G1ka2zItL-dGsbv6TuLhuwMsLgMXi4jNGG8pfnJATH05Fb86ca85-BJd1scFF6-aQ21fpOYV_rPEL46OhEA</recordid><startdate>20040401</startdate><enddate>20040401</enddate><creator>Sandager-Nielsen, Karin</creator><creator>Andersen, Maibritt B</creator><creator>Sager, Thomas N</creator><creator>Werge, Thomas</creator><creator>Scheel-Krüger, Jørgen</creator><general>Elsevier Inc</general><general>Elsevier Science</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>7U7</scope><scope>C1K</scope><scope>7X8</scope></search><sort><creationdate>20040401</creationdate><title>Effects of postnatal anoxia on striatal dopamine metabolism and prepulse inhibition in rats</title><author>Sandager-Nielsen, Karin ; Andersen, Maibritt B ; Sager, Thomas N ; Werge, Thomas ; Scheel-Krüger, Jørgen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c476t-5a7cb60b421f992f5f2d10af0ae4c96a00a17e3b90940b62c34218b662465ab83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Age Factors</topic><topic>Animal model</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Anoxia</topic><topic>Biological and medical sciences</topic><topic>Corpus Striatum - metabolism</topic><topic>Dopamine</topic><topic>Dopamine - metabolism</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hypoxia, Brain - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>N-acetylaspartate</topic><topic>Neuropharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Prepulse inhibition</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychology. 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Epidemiological observations point to oxygen deficiencies during delivery as one of the early risk factors for developing schizophrenia. The aim of the present study was to examine the effect of postnatal anoxia in rats. Anoxia was experimentally induced by placing 9-day-old rat pups for 6 min in a chamber saturated with 100% nitrogen (N
2). Exposure to anoxia on postnatal day (PND) 9 resulted in significantly reduced subcortical dopamine metabolism and turnover, as measured by striatal 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) concentrations. Furthermore, in the anoxic group only, striatal HVA concentrations were negatively correlated to prefrontal cortical
N-acetylaspartate (NAA) levels. Similar findings of distorted prefrontal–subcortical interactions have recently been reported in schizophrenic patients. There was no effect of postnatal anoxia on either baseline or
d-amphetamine-induced deficit in the prepulse inhibition (PPI) paradigm in adulthood. Accordingly, although oxygen deficiency early in life has been discussed as vulnerability factor in developing schizophrenia, exposure to postnatal anoxia in the rat does not show clear-cut phenomenological similarities with the disorder.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>15099922</pmid><doi>10.1016/j.pbb.2004.01.017</doi><tpages>8</tpages></addata></record> |
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| subjects | Age Factors Animal model Animals Animals, Newborn Anoxia Biological and medical sciences Corpus Striatum - metabolism Dopamine Dopamine - metabolism Female Fundamental and applied biological sciences. Psychology Hypoxia, Brain - metabolism Male Medical sciences N-acetylaspartate Neuropharmacology Pharmacology. Drug treatments Prepulse inhibition Psychology. Psychoanalysis. Psychiatry Psychology. Psychophysiology Rats Rats, Wistar Reflex, Startle - physiology Schizophrenia |
| title | Effects of postnatal anoxia on striatal dopamine metabolism and prepulse inhibition in rats |
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