Universidad Argentina John F Kennedy, Buenos Aires, Argentina.
Nutr Neurosci. 2012 May;15(3):103-10. doi: 10.1179/1476830511Y.0000000026.
Perinatal asphyxia (PA) is a medical condition associated with a high short-term morbimortality and different long-term neurological diseases. In previous work we have observed at 6 months post-synaptic densities (PSDs) alterations compatible with neurodegeneration highly correlated with the increment in the ubiquitination. Although alterations in the synaptic organization and function have been related with neuronal death after hypoxia, little is known about the synaptic changes in young animals exposed to PA. The main aim of this work is to study the PSDs changes in striatum of 30-day-old rats subjected to PA. Using two-dimensional electron microscopic analyses of synapses staining with ethanolic phosphotungstic acid we observed an increment of PSD thickness in severe hypoxic rats. These data are consistent with the western blot analysis that showed an increment in ubiquitination levels in the synapses of severe hypoxic rat. We did observe any alterations neither in synaptic structure nor in ubiquitinization in mild asphyctic rats. These data suggest that hypoxia might cause early misfolding and aggregation of synaptic proteins in severe anoxic animas that could induce long-term neurodegeneration.
围产期窒息（PA）是一种与高短期发病率和死亡率以及不同长期神经系统疾病相关的医学病症。在之前的研究中，我们观察到突触后密度（PSD）的改变，这些改变与神经退行性变兼容，并且与泛素化的增加高度相关。尽管缺氧后突触组织和功能的改变与神经元死亡有关，但对于暴露于 PA 的年轻动物的突触变化知之甚少。这项研究的主要目的是研究在 PA 作用下 30 日龄大鼠纹状体中的 PSDs 变化。通过用乙醇磷钨酸对突触进行二维电子显微镜分析，我们观察到严重缺氧大鼠 PSD 厚度增加。这些数据与 Western blot 分析一致，该分析显示严重缺氧大鼠突触中的泛素化水平增加。我们在轻度窒息大鼠中没有观察到任何突触结构或泛素化的改变。这些数据表明，缺氧可能导致严重缺氧动物中突触蛋白的早期错误折叠和聚集，从而导致长期神经退行性变。
