論文

査読有り
2004年

Serial analysis of gene expression in methamphetamine- and phencyclidine-treated rodent cerebral cortices are there common mechanisms?

CURRENT STATUS OF DRUG DEPENDENCE / ABUSE STUDIES: CELLULAR AND MOLECULAR MECHANISMS OF DRUGS OF ABUSE AND NEUROTOXICITY
  • Y Ouchi
  • ,
  • Y Kubota
  • ,
  • C Ito

1025
開始ページ
57
終了ページ
61
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1196/annals.1316.007
出版者・発行元
NEW YORK ACAD SCIENCES

Pharmacological actions of methamphetamine (METH) and phencyclidine (PCP) are different, but both of them can induce similar psychiatric disorders including abuse, intoxication, withdrawal, and psychotic symptoms like those of schizophrenia. These mental disorders are caused not only by their direct pharmacological effects, but also by secondary brain damage containing gene expression changes. In order to broadly grasp these alterations, we used serial analysis of gene expression (SAGE), a transcriptome analysis. We analyzed three cDNA libraries from cerebral cortices of saline (1 mL/kg)-, METH (4 mg/kg)-, or PCP (10 mg/kg)-treated Wistar rats (one hour after i.p. administration). The numbers of total tags were about 50,000 in each library, and approximately 18,000 kinds of tags were identified respectively. From the comparisons of three groups, we found both METH- and PCP-reactive genes. Upregulated genes contained calmodulin 2, stromal cell-derived factor receptor 1, brain-specific angiogenesis inhibitor 1-associated protein 2, ras homologue enriched in brain, basigin and thyrotropin-releasing hormone receptor. Downregulated genes contained lipocalin 2, aldolase A, importin 13, fatty acid binding protein 3, and glycine receptor alpha2 subunit These data suggest important clues of common molecular basis in METH- and PCP-related psychiatric disorders.

リンク情報
DOI
https://doi.org/10.1196/annals.1316.007
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000226975200007&DestApp=WOS_CPL
ID情報
  • DOI : 10.1196/annals.1316.007
  • ISSN : 0077-8923
  • Web of Science ID : WOS:000226975200007

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