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Protein malnutrition during gestation and early life decreases neuronal size in the medial prefrontal cortex of post-pubertal rats

机译:妊娠和早期生命期间的蛋白质营养不良会降低青春期后大鼠前额内侧皮层的神经元大小

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摘要

Retrospective studies in human populations indicate that protein deprivation during pregnancy and early life (early protein malnutrition, EPM) is associated with cognitive impairments, learning disabilities and may represent a risk factor for the late onset of some psychiatric disorders, fundamentally schizophrenia, a condition where the prefrontal cortex plays an important role. The purpose of this study was to analyze whether EPM affects structural aspects of the rat medial prefrontal cortex (mPFC), such as cortical volume, neuronal density and neuronal soma size, which seem altered in patients with schizophrenia. For this, a rat model of EPM (5% casein from conception to postnatal day 60) was adopted and the rat mPFC volume, total number of neurons and average neuronal volume were evaluated on postnatal day 60 (post-pubertal animals) by histo- and immunohistochemical techniques using unbiased stereological analysis. EPM did not alter the number of NeuN+ neurons in the rat mPFC. However, a very significant decrease in mPFC volume and average neuronal size was observed in malnourished rats. Although the present study does not establish causal relationships between malnutrition and schizophrenia, our results may indicate a similar structural phenomenon in these two situations.
机译:人群的回顾性研究表明,怀孕和生命早期蛋白质缺乏(早期蛋白质营养不良,EPM)与认知障碍,学习障碍有关,并且可能是某些精神疾病(基本上是精神分裂症)迟发的危险因素。前额叶皮层起着重要作用。这项研究的目的是分析EPM是否会影响大鼠精神分裂症患者的前内侧额叶皮层(mPFC)的结构方面,例如皮质体积,神经元密度和神经元体大小。为此,采用了EPM大鼠模型(从受孕到出生后60天为5%酪蛋白),并在出生后60天(青春期后的动物)通过组织学方法评估了大鼠的mPFC体积,神经元总数和平均神经元体积。和免疫组织化学技术,使用无偏见的立体分析。 EPM不会改变大鼠mPFC中NeuN +神经元的数量。但是,在营养不良的大鼠中,mPFC的体积和平均神经元大小明显减少。尽管本研究并未建立营养不良与精神分裂症之间的因果关系,但我们的结果可能表明这两种情况下存在类似的结构现象。

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