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    TorsinA, the gene linked to early-onset dystonia, is upregulated by the dopaminergic toxin MPTP in mice (2004)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Kuner, Rohini
    Teismann, Peter
    Trutzel, Annette
    Naim, Jomana
    Richter, Angelika
    Schmidt, Nicole
    Bach, Alfred
    Ferger, Boris
    Schneider, Armin
    Quelle
    Neuroscience Letters; 355(1/2) — S. 126–130
    ISSN: 0304-3940
    Sprache
    Englisch
    Verweise
    Pubmed: 14729251
    Kontakt
    Institut für Pharmakologie und Toxikologie

    Koserstr. 20
    14195 Berlin
    +49 30 838 53221
    pharmakologie@vetmed.fu-berlin.de

    Abstract / Zusammenfassung

    Early-onset torsion dystonias are caused by a mutation in TorsinA, a protein widely expressed in the nervous system. Here we report the cloning of the murine TorsinA cDNA and a mRNA in situ hybridization analysis of the expression patterns of TorsinA over developmental periods relevant to the etiology of early-onset dystonias. Several studies have demonstrated a functional involvement of the nigrostriatal dopaminergic system in pathological mechanisms underlying dystonia. In this study, we show that the expression of TorsinA is significantly increased in the brain within hours of treatment with the dopaminergic toxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in mice, suggesting that the TorsinA gene is regulated by cellular stress. These results provide insights into the pathophysiology of early-onset dystonia and strengthen links between the dopaminergic system and dystonia.