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Zhong N Kim CY Rizzu P Geula C Porter DR Pothos EN Squitieri F Heutink P Xu J 《The Journal of biological chemistry》2006,281(30):20940-20948
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Dong L Zhang X Fu X Zhang X Gao X Zhu M Wang X Yang Z Jensen ON Saarikettu J Yao Z Silvennoinen O Yang J 《The Journal of biological chemistry》2011,286(5):3451-3459
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Nigrostriatal dopaminergic deficits and hypokinesia caused by inactivation of the familial Parkinsonism-linked gene DJ-1 总被引:1,自引:0,他引:1
Goldberg MS Pisani A Haburcak M Vortherms TA Kitada T Costa C Tong Y Martella G Tscherter A Martins A Bernardi G Roth BL Pothos EN Calabresi P Shen J 《Neuron》2005,45(4):489-496
The manifestations of Parkinson's disease are caused by reduced dopaminergic innervation of the striatum. Loss-of-function mutations in the DJ-1 gene cause early-onset familial parkinsonism. To investigate a possible role for DJ-1 in the dopaminergic system, we generated a mouse model bearing a germline disruption of DJ-1. Although DJ-1(-/-) mice had normal numbers of dopaminergic neurons in the substantia nigra, evoked dopamine overflow in the striatum was markedly reduced, primarily as a result of increased reuptake. Nigral neurons lacking DJ-1 were less sensitive to the inhibitory effects of D2 autoreceptor stimulation. Corticostriatal long-term potentiation was normal in medium spiny neurons of DJ-1(-/-) mice, but long-term depression (LTD) was absent. The LTD deficit was reversed by treatment with D2 but not D1 receptor agonists. Furthermore, DJ-1(-/-) mice displayed hypoactivity in the open field. Collectively, our findings suggest an essential role for DJ-1 in dopaminergic physiology and D2 receptor-mediated functions. 相似文献
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