【摘 要】
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We previously found that alpha-Synuclein (Syn) localized not only in neuclei but also in axons and cytoplasm, especially enriched in mitochondria.Despite of accumulating evidence showing that overexpr
【机 构】
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Beijing Institute for Neuroscience, Capital Medical University (CMU), Beijing Center of Neural Regen
【出 处】
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中国神经科学学会第九届全国学术会议暨第五届会员代表大会
论文部分内容阅读
We previously found that alpha-Synuclein (Syn) localized not only in neuclei but also in axons and cytoplasm, especially enriched in mitochondria.Despite of accumulating evidence showing that overexpression of Syn could partly mimic the symptom of Parkisons disease (PD), the exact mechanism remains elusive.To find out the subcelluar localization of Syn in substantia nigra (SN) neurons especially on mitochondria and its effect on mitochondria in Syn induced PD rats model may help explain the pathogenesis of Syn in PD.In the present study, the synuclein gene was introduced into the SN of rats using recombinant adeno-associtaed viral (rAAV) vector.Using immunogold electron microscopic technique, we found that the density of Syn-positive gold particles was greater in both substantia nigra and striatum in PD rat model than in the control group.To compare the distribution of Syn in different cell compartment with the control group, the density of Syn-positive gold particles was greater in neuclei, axons, cytoplasms, especially mitochondria in SN of PD rat model, while the density of gold particles decreased to zero in pre-synaptic terminals.Differently with the SN regeon, the density of gold particles increased mainly in pre-synaptic terminals, cytoplasm and neucleus in PD rat model, with no difference in axons and mitochondria.
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