Fetal Programming and Hydro-electrolyte Metabolism Laboratory, Internal Medicine Department, School of Medicine, State University of Campinas, Campinas, SP, Brazil.
ICVS/3B's-PT Government Associate Laboratory, Braga, Guimarães, Portugal.
Nutr Neurosci. 2023 Nov;26(11):1103-1119. doi: 10.1080/1028415X.2022.2131064. Epub 2022 Nov 4.
Gestational protein intake restriction-induced long-lasting harmful outcomes in the offspring's organs and systems. However, few studies have focused on this event's impact on the brain's structures and neurochemical compounds.
The present study investigated the effects on the amygdala neurochemical composition and neuronal structure in gestational protein-restricted male rats' offspring.
Dams were maintained on isocaloric standard rodent laboratory chow with regular protein [NP, 17%] or low protein content [LP, 6%]. Total cells were quantified using the Isotropic fractionator method, Neuronal 3D reconstruction, and dendritic tree analysis using the Golgi-Cox technique. Western blot and high-performance liquid chromatography performed neurochemical studies.
The gestational low-protein feeding offspring showed a significant decrease in birth weight up to day 14, associated with unaltered brain weight in youth or adult progenies. The amygdala cell numbers were unchanged, and the dendrites length and dendritic ramifications 3D analysis in LP compared to age-matched NP progeny. However, the current study shows reduced amygdala content of norepinephrine, epinephrine, and dopamine in LP progeny. These offspring observed a significant reduction in the amygdala glucocorticoid (GR) and mineralocorticoid (MR) receptor protein levels. Also corticotrophin-releasing factor (CRF) amygdala protein content was reduced in 7 and 14-day-old LP rats.
The observed amygdala neurochemical changes may represent adaptation during embryonic development in response to elevated fetal exposure to maternal corticosteroid levels. In this way, gestational malnutrition stress can alter the amygdala's neurochemical content and may contribute to known behavioral changes induced by gestational protein restriction.
妊娠期蛋白质摄入限制会对后代的器官和系统造成持久的有害影响。然而，很少有研究关注这种事件对大脑结构和神经化学物质的影响。
本研究旨在探讨妊娠期蛋白质限制对雄性子代大鼠杏仁核神经化学组成和神经元结构的影响。
给予孕鼠等热量标准实验室鼠粮，蛋白质含量正常[NP，17%]或低[LP，6%]。使用等向分数化方法定量总细胞数，使用 Golgi-Cox 技术进行神经元 3D 重建和树突分析。使用 Western blot 和高效液相色谱进行神经化学研究。
妊娠期低蛋白喂养的后代在出生后第 14 天体重显著下降，而青年或成年后代的脑重未受影响。杏仁核细胞数量无变化，LP 组与年龄匹配的 NP 后代相比，其树突长度和树突分支 3D 分析无差异。然而，本研究显示 LP 后代的杏仁核去甲肾上腺素、肾上腺素和多巴胺含量减少。这些后代的杏仁核糖皮质激素（GR）和盐皮质激素（MR）受体蛋白水平显著降低。此外，7 天和 14 天 LP 大鼠的杏仁核促肾上腺皮质释放因子（CRF）蛋白含量也降低。
观察到的杏仁核神经化学变化可能代表了胚胎发育过程中对母体皮质醇水平升高的胎儿暴露的适应。因此，妊娠期营养不良应激可以改变杏仁核的神经化学物质含量，并可能导致已知的妊娠期蛋白质限制引起的行为变化。
