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首页> 外文期刊>Neuroreport >A novel mechanism of dopamine neurotoxicity involving the peripheral extracellular and the plasma membrane dopamine transporter.
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A novel mechanism of dopamine neurotoxicity involving the peripheral extracellular and the plasma membrane dopamine transporter.

机译：多巴胺神经毒性的新机制涉及外周细胞外和质膜多巴胺转运蛋白。

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摘要

Chinese hamster ovary cells stably expressing a rat dopamine transporter (designated D8 cells) and neuroblastoma SK-N-SH cells were used as two model systems to study dopamine neurotoxicity. Within 24 h, 1-10 mM dopamine induced D8 cells into apoptosis while 20-200 microM dopamine induced SK-N-SH cells into cell death. The viability of both cell types decreased in a dose-dependent manner. However, the dopamine uptake activity of D8 cells at 10 mM was not significantly higher than the uptake at 100 microM, suggesting that it was not the high concentration of intracellular dopamine that induced D8 cells into apoptosis, but rather dopamine found in the extracellular space. Furthermore, cocaine, an inhibitor of dopamine uptake, could not block cell death induced by dopamine. Forskolin, an agonist of protein kinase A (PKA), stimulated dopamine uptake in D8 cells and blocked apoptosis induced by the drug. These results suggest that the dopamine transporter mediates a dopamine-dependant apoptotic signal transduction pathway that is independent of dopamine uptake into the cell.
机译：稳定表达大鼠多巴胺转运蛋白的中国仓鼠卵巢细胞（称为D8细胞）和成神经细胞瘤SK-N-SH细胞用作研究多巴胺神经毒性的两个模型系统。在24小时内，1-10 mM多巴胺诱导D8细胞凋亡，而20-200 microM多巴胺诱导SK-N-SH细胞死亡。两种细胞类型的活力均以剂量依赖性方式降低。然而，D8细胞在10 mM时的多巴胺摄取活性并不明显高于100 microM时的摄取，表明不是高浓度的细胞内多巴胺会诱导D8细胞凋亡，而是在细胞外空间中发现多巴胺。此外，可卡因是多巴胺摄取的抑制剂，不能阻止多巴胺诱导的细胞死亡。蛋白激酶A（PKA）的激动剂Forskolin刺激D8细胞吸收多巴胺，并阻断了该药物诱导的细胞凋亡。这些结果表明，多巴胺转运蛋白介导了独立于细胞中多巴胺摄取的多巴胺依赖性凋亡信号转导途径。

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