中文摘要：

包含神经蛋白质 -synuclein 的包括身体(-syn) 在几 neurodegenerative 疾病被观察，包括 Parkinson 的疾病(PD ) 。而且，在老鼠大脑的 -syn 的在表示上部分由在 substantia nigra (SN ) 触发 dopaminergic 神经原的退化模仿 neuropathological 和 PD 的行为的特征。Mitochondrial 机能障碍对 PD 致病也中央，并且 -syn 在线粒体被发现。然而， -syn-induced neurotoxicity 的精确机制留下逃犯。检验 -syn-induced neurodegeneration 的潜在的机制，我们在用 recombinant 的老鼠的 SN 的过去表示的 -syn 联系 adeno 的病毒的向量(rAAV-syn ) 。把结果标记的 Immunohistochemical 和 immunogold 显示 -syn 在向量注射以后在 SN 和 striatum 是成功地过去表示的。酷氨酸的数字 hydroxylase 积极(dopaminergic ) 神经原显著地在当时，与 rAAV-syn 注射的老鼠被减少与控制老鼠相比。与控制老鼠相比， -syn-conjugated 金牌粒子的密度在轴突是更大的，细胞质，原子核，并且尤其是另外在在 rAAV-syn-injected 老鼠的 SN 神经原的线粒体。另外，有 rAAV-syn 的 SN 神经原 transfected 与不连续的外部膜和内部像液泡的结构展出了肿的线粒体，强烈建议 -syn-induced mitochondrial 机能障碍。在 rAAV-syn-injected 老鼠的线粒体也在 autophagosomes 被观察。有电压依赖者阴离子隧道 1 的 -Syn co-immunoprecipitated (VDAC1 ) ，导致 mitochondrial 解开的 mitochondrial 渗透转变毛孔(mPTP ) 的一个部件和 apoptosis。-syn 的在表示上可以通过和 mitochondrial VDAC1 的一个相互作用引起 dopaminergic 神经原的退化，它导致 mPTP 激活，解开的 mitochondrial，和房间死亡。

英文摘要：

Inclusion bodies containing the neural protein α-synuclein （et-syn） are observed in several neurodegenerative diseases, including Parkinson＇s disease （PD）. Furthermore, over-expression of α-syn in rat brain partly mimics the neuropathological and behavioral features of PD by triggering the degeneration of dopaminergic neurons in the substantia nigra （SN）. Mitochondrial dysfunction is also central to PD pathogenesis, and α-syn is found in the mitochondria. However, the precise mechanisms of α-syninduced neurotoxicity remain elusive. To examine the potential mechanisms of α-syn-induced neurodegeneration, we over-expressed α-syn in the SN of rats using a recombinant adeno-associated viral vector （rAAV-syn）. Immunohistochemical and immunogold labeling results indicated that α-syn was successfully over-expressed in the SN and striatum after vector injection. The number of tyrosine hydroxylase-positive （dopaminergic） neurons was significantly reduced in rats injected with rAAV-syn when compared with control rats. Compared with control rats, the density of α-syn-conjugated gold particles was greater in the axons, cytoplasm, nuclei, and notably also in the mitochondria of SN neurons in rAAV-syn-injected rats. In addition, SN neurons transfected with rAAV-syn exhibited swollen mitochondria with discontinuous outer membranes and internal vacuole-like structures, strongly suggesting oL-syn-induced mitochondrial dysfunction. Mitochondria in rAAV-syn-injected rats were also observed in autophago- somes, ol-Syn co-immunoprecipitated with voltagedependent anion channel 1 （ArDAC1）, a component of the mitochondrial permeability transition pore （mPTP） that induces mitochondrial uncoupling and apoptosis. Overexpression of α-syn may cause the degeneration of dopaminergic neurons through an interaction with mitochondrial VDACl, which leads to mPTP activation, mito- chondrial uncoupling, and cell death.