【摘要】 目的探讨α-突触核蛋白(α-Syn)和β淀粉样蛋白(Aβ1-42)寡聚体对小鼠原代皮质、海马神经细胞突触功能和活性的影响。方法分别采用二甲基亚砜、Aβ42-1寡聚体、α-Syn、Aβ1-42寡聚体、α-Syn+Aβ42-1寡聚体、α-Syn+Aβ1-42寡聚体干预小鼠原代皮质和海马神经元,按不同干预方法分为6组。干预24 h后用免疫荧光、FM1-43染色法检测神经元的突触数量及活性,同时用Western blot法检测半胱氨酸伸展蛋白α(CSPα)表达。结果与其余5组比较,α-Syn+Aβ1-42寡聚体组可使突触相关CSPα表达明显下降(P<0.01)、与突触数目相关的突触蛋白Ⅰ明显降低(P<0.01),同时突触活性也明显下降(P<0.01)。结论α-Syn和Aβ1-42寡聚体可协同作用于神经元,减少CSPα表达,降低细胞突触数目及其功能。更多还原

【Abstract】 Aim To explore the effect of α-synuclein(α-syn) and β-amyloid 1-42(Aβ 1-42) on the synapses of primary cultured cortical and hippocampal neurons. Methods Primary cultured neurons were divided into 6 groups, each group was treated by DMSO, Aβ 42-1, α-syn, Aβ 1-42, α-syn+Aβ 42-1 and α-syn+Aβ 1-42, respectively. After 24 hours incubation, the numbers and the activity of synapses were detected by the double immunofluorescence dying and FM1-43 dying, meanwhile the expression of cysteine string protein-α(CSPα) were analyzed by Western blot. Results Compared with 5 other groups, α-syn+Aβ 1-42 group could significantly decrease the expression of CSPα(P<0.01),and synapse-associated synapsin I could significantly decrease(P<0.01), as well as the synaptic activity(P<0.01). Conclusion α-syn together with Aβ 1-42 could result in synergistic effect, which would decrease the expression of CSPα and then interact with synapses. The process finally reduced the function and activity of primary cultured cortical and hippocampal neurons.更多还原