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建立孕期酒精暴露(PAE)模型,研究孕期酒精暴露对小鼠视皮质突触数量的影响。利用免疫荧光染色技术标记对照组与PAE模型组(低剂量和高剂量)子鼠出生后0、7、14及30d视皮质突触前体的synaptophysin蛋白表达,以此来代表突触,观察其数密度变化,并利用Western blotting检测对各实验组子代小鼠视皮质synaptophysin的表达量进行半定量分析。突触数密度值统计学分析显示:对照组、低剂量和高剂量组间比较差异显著(P<0.05),0、7、14及30d差异显著(P<0.05),年龄与剂量之间存在交互作用(P<0.05)且剂量的影响作用更大。Western blotting检测结果与免疫荧光统计结果一致。这表明PAE对突触的影响具有长时程效应和剂量相关性,突触丢失的长时程放大效应可能是患儿精神发育迟滞和记忆力下降的主要原因。
Establishment of pregnancy alcohol exposure (PAE) model to study the influence of alcohol exposure during pregnancy on visual cortex synapses in mice. Immunofluorescence staining was used to mark the synaptophysin protein expression of visual cortex synapse precursors at 0, 7, 14 and 30 days after birth in PAE model group (low dose and high dose) The density of synaptophysin was detected by Western blotting. The expression of synaptophysin was detected by semi-quantitative analysis. Statistical analysis of the number density of synapses showed that there was significant difference between the control group, low dose and high dose groups (P <0.05), and the difference was significant at 0, 7, 14 and 30 d (P <0.05) Interaction (P <0.05) and dose effects were greater. Western blotting results were consistent with immunofluorescence statistics. This suggests that PAE has long-term and dose-dependent effects on synapses. The long-term effects of synaptic loss may be responsible for mental retardation and memory loss in children.