Neuronal cell death mediated by mitochondria

谷氨酸的神经毒性作用至少部分涉及线粒体膜电位的破坏、MPTP的编配、线粒体游离钙离子水平和UCP2在大鼠海马神经元和皮质神经元的表达。在具有获得性NMDAR通道和UCP2高表达的HEK293细胞中，暴露于NMDA后，线粒体游离钙水平比UCP2高表达的细胞更显著地增加，并且细胞死亡更严重。因此，UCP2可作为NMDAR介导的神经毒性的决定因子，其机制与调节神经元线粒体游离钙水平有关。

Glutamate neurotoxicity was found to at least in part involve mitochondrial membrane potential disruption, mPTP orchestration, mitochondrial free Ca^<2+> levels and UCP2 expression in rat hippocampal and cortical neurons. In HEK293 cells with acquired NMDAR channels and overexpressed UCP2, a more marked increase was seen in mitochondrial free Ca^<2+> levels, in addition to more severe cell death, after the exposure to NMDA than in cells without UCP2 overexpression. Accordingly, UCP2 could play a role as a determinant of the neurotoxicity mediated by NMDAR through a mechanism related to the modulation of mitochondrial free Ca^<2+> levels in neurons.