pubmed-article:17457314 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17457314 | lifeskim:mentions | umls-concept:C0001675 | lld:lifeskim |
pubmed-article:17457314 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:17457314 | lifeskim:mentions | umls-concept:C0599779 | lld:lifeskim |
pubmed-article:17457314 | lifeskim:mentions | umls-concept:C0036341 | lld:lifeskim |
pubmed-article:17457314 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
pubmed-article:17457314 | lifeskim:mentions | umls-concept:C1417836 | lld:lifeskim |
pubmed-article:17457314 | lifeskim:mentions | umls-concept:C0392756 | lld:lifeskim |
pubmed-article:17457314 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
pubmed-article:17457314 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
pubmed-article:17457314 | pubmed:issue | 8 | lld:pubmed |
pubmed-article:17457314 | pubmed:dateCreated | 2007-7-26 | lld:pubmed |
pubmed-article:17457314 | pubmed:abstractText | The transcription factor Nurr1 (NR4A2) has been found to play a critical role in the development of midbrain dopaminergic neurons. Nurr1 heterozygous (+/-) male and female mice expressing 35-40% of normal levels of Nurr1 were generated and examined in animal models related to symptoms of schizophrenia. The Nurr1 (+/-) mice displayed hyperactivity in a novel environment, which persisted after administration of the dopamine-mimetic amphetamine and the N-methyl-D-aspartate receptor antagonist phencyclidine. The Nurr1 (+/-) mice were deficient in the retention of emotional memory and showed an enhanced response to swim stress. In addition, Nurr1 (+/-) male mice displayed a reduced dopamine turnover in the striatum and an enhanced dopamine turnover in the prefrontal cortex, while female mice showed an opposite pattern. These results show that Nurr1 (+/-) mice display a pattern of behaviors indicative of potential relevance for symptoms of schizophrenia combined with a gender-specific abnormal dopamine transmission in the striatum and prefrontal cortex, respectively. This suggests that the Nurr1 mutant mouse may be a potential animal model for studies on some of the behavioral and molecular mechanisms underlying schizophrenia. | lld:pubmed |
pubmed-article:17457314 | pubmed:language | eng | lld:pubmed |
pubmed-article:17457314 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17457314 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:17457314 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17457314 | pubmed:month | Aug | lld:pubmed |
pubmed-article:17457314 | pubmed:issn | 1359-4184 | lld:pubmed |
pubmed-article:17457314 | pubmed:author | pubmed-author:OgrenS OSO | lld:pubmed |
pubmed-article:17457314 | pubmed:author | pubmed-author:RojasPP | lld:pubmed |
pubmed-article:17457314 | pubmed:author | pubmed-author:HonyKK | lld:pubmed |
pubmed-article:17457314 | pubmed:author | pubmed-author:PerlmannTT | lld:pubmed |
pubmed-article:17457314 | pubmed:author | pubmed-author:JoodmardiEE | lld:pubmed |
pubmed-article:17457314 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:17457314 | pubmed:volume | 12 | lld:pubmed |
pubmed-article:17457314 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17457314 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17457314 | pubmed:pagination | 756-66 | lld:pubmed |
pubmed-article:17457314 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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pubmed-article:17457314 | pubmed:year | 2007 | lld:pubmed |
pubmed-article:17457314 | pubmed:articleTitle | Adult mice with reduced Nurr1 expression: an animal model for schizophrenia. | lld:pubmed |
pubmed-article:17457314 | pubmed:affiliation | Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden. | lld:pubmed |
pubmed-article:17457314 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17457314 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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