Amaral A C, Lister J P, Rueckemann J W, Wojnarowicz M W, McGaughy J A, Mokler D J, Galler J R, Rosene D L, Rushmore R J
Department of Anatomy & Neurobiology, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.
Department of Pathology and Laboratory Medicine, University of California Los Angeles, Los Angeles, CA, USA.
Nutr Neurosci. 2025 Mar;28(3):333-346. doi: 10.1080/1028415X.2024.2371256. Epub 2024 Aug 1.
Prenatal protein malnutrition produces anatomical and functional changes in the developing brain that persist despite immediate postnatal nutritional rehabilitation. Brain networks of prenatally malnourished animals show diminished activation of prefrontal areas and an increased activation of hippocampal regions during an attentional task [1]. While a reduction in cell number has been documented in hippocampal subfield CA1, nothing is known about changes in neuron numbers in the prefrontal or parahippocampal cortices.
In the present study, we used unbiased stereology to investigate the effect of prenatal protein malnutrition on the neuron numbers in the medial prefrontal cortex and the cortices of the parahippocampal region that comprise the larger functional network.
Results show that prenatal protein malnutrition does not cause changes in the neuronal population in the medial prefrontal cortex of adult rats, indicating that the decrease in functional activation during attentional tasks is not due to a reduction in the number of neurons. Results also show that prenatal protein malnutrition is associated with a reduction in neuron numbers in specific parahippocampal subregions: the medial entorhinal cortex and presubiculum.
The affected regions along with CA1 comprise a tightly interconnected circuit, suggesting that prenatal malnutrition confers a vulnerability to specific hippocampal circuits. These findings are consistent with the idea that prenatal protein malnutrition produces a reorganization of structural and functional networks, which may underlie observed alterations in attentional processes and capabilities.
产前蛋白质营养不良会在发育中的大脑中产生解剖学和功能上的变化,即便在出生后立即进行营养康复,这些变化仍会持续存在。产前营养不良动物的脑网络在注意力任务期间显示前额叶区域的激活减少,而海马区域的激活增加[1]。虽然海马体CA1亚区的细胞数量减少已有记录,但对于前额叶或海马旁皮质中神经元数量的变化却一无所知。
在本研究中,我们使用无偏倚立体学方法来研究产前蛋白质营养不良对内侧前额叶皮质以及构成更大功能网络的海马旁区域皮质中神经元数量的影响。
结果表明,产前蛋白质营养不良不会导致成年大鼠内侧前额叶皮质中神经元数量的变化,这表明注意力任务期间功能激活的减少并非由于神经元数量的减少。结果还表明,产前蛋白质营养不良与海马旁特定亚区域(内侧内嗅皮质和前下托)的神经元数量减少有关。
受影响的区域与CA1一起构成了一个紧密相连的回路,这表明产前营养不良使特定的海马回路易受影响。这些发现与产前蛋白质营养不良会导致结构和功能网络重组的观点一致,而这可能是观察到的注意力过程和能力改变的基础。