pubmed-article:18184313 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:18184313 | lifeskim:mentions | umls-concept:C0034798 | lld:lifeskim |
pubmed-article:18184313 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
pubmed-article:18184313 | lifeskim:mentions | umls-concept:C1514758 | lld:lifeskim |
pubmed-article:18184313 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:18184313 | pubmed:dateCreated | 2008-1-10 | lld:pubmed |
pubmed-article:18184313 | pubmed:abstractText | Exposure to drugs of abuse activates gene expression and protein synthesis that result in long-lasting adaptations in striatal signaling. Therefore, identification of the transcription factors that couple drug exposure to gene expression is of particular importance. Members of the nuclear factor of activated T-cells (NFATc) family of transcription factors have recently been implicated in shaping neuronal function throughout the rodent nervous system. Here we demonstrate that regulation of NFAT-mediated gene expression may also be a factor in drug-induced changes to striatal functioning. In cultured rat striatal neurons, stimulation of D1 dopamine receptors induces NFAT-dependent transcription through activation of L-type calcium channels. Additionally, the genes encoding inositol-1,4,5-trisphosphate receptor type 1 and glutamate receptor subunit 2 are regulated by striatal NFATc4 activity. Consistent with these in-vitro data, repeated exposure to cocaine triggers striatal NFATc4 nuclear translocation and the up-regulation of inositol-1,4,5-trisphosphate receptor type 1 and glutamate receptor subunit 2 gene expression in vivo, suggesting that cocaine-induced increases in gene expression may be partially mediated through activation of NFAT-dependent transcription. Collectively, these findings reveal a novel molecular pathway that may contribute to the enduring modifications in striatal functioning that occur following the administration of drugs of abuse. | lld:pubmed |
pubmed-article:18184313 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18184313 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18184313 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18184313 | pubmed:language | eng | lld:pubmed |
pubmed-article:18184313 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18184313 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:18184313 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18184313 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:18184313 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18184313 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18184313 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18184313 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18184313 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18184313 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18184313 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18184313 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18184313 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18184313 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:18184313 | pubmed:month | Jan | lld:pubmed |
pubmed-article:18184313 | pubmed:issn | 1460-9568 | lld:pubmed |
pubmed-article:18184313 | pubmed:author | pubmed-author:AravamudanBha... | lld:pubmed |
pubmed-article:18184313 | pubmed:author | pubmed-author:ThomasMark... | lld:pubmed |
pubmed-article:18184313 | pubmed:author | pubmed-author:MermelsteinPa... | lld:pubmed |
pubmed-article:18184313 | pubmed:author | pubmed-author:GrothRachel... | lld:pubmed |
pubmed-article:18184313 | pubmed:author | pubmed-author:WeickJason... | lld:pubmed |
pubmed-article:18184313 | pubmed:author | pubmed-author:BradleyKather... | lld:pubmed |
pubmed-article:18184313 | pubmed:author | pubmed-author:KlugJason RJR | lld:pubmed |
pubmed-article:18184313 | pubmed:author | pubmed-author:LuomaJessie... | lld:pubmed |
pubmed-article:18184313 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:18184313 | pubmed:volume | 27 | lld:pubmed |
pubmed-article:18184313 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:18184313 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:18184313 | pubmed:pagination | 31-42 | lld:pubmed |
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pubmed-article:18184313 | pubmed:year | 2008 | lld:pubmed |
pubmed-article:18184313 | pubmed:articleTitle | D1 dopamine receptor activation of NFAT-mediated striatal gene expression. | lld:pubmed |
pubmed-article:18184313 | pubmed:affiliation | Department of Neuroscience, University of Minnesota, 6-145 Jackson Hall, 321 Church Street, S.E., Minneapolis, MN 55455, USA. | lld:pubmed |
pubmed-article:18184313 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:18184313 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
pubmed-article:18184313 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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