Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati, Cincinnati OH, USA.
Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati, Cincinnati OH, USA.
Front Neuroendocrinol. 2017 Oct;47:109-122. doi: 10.1016/j.yfrne.2017.07.007. Epub 2017 Jul 20.
Maternal malnutrition significantly increases offspring risk for both metabolic and neurodevelopmental disorders. Animal models of maternal malnutrition have identified behavioral changes in the adult offspring related to executive function and reward processing. Together, these changes in executive and reward-based behaviors likely contribute to the etiology of both metabolic and neurodevelopmental disorders associated with maternal malnutrition. Concomitant with the behavioral effects, maternal malnutrition alters offspring expression of reward-related molecules and inflammatory signals in brain pathways that control executive function and reward. Neuroimmune pathways and microglial interactions in these specific brain circuits, either in early development or later in adulthood, could directly contribute to the maternal malnutrition-induced behavioral phenotypes. Understanding these mechanisms will help advance treatment strategies for metabolic and neurodevelopmental disorders, especially noninvasive dietary supplementation interventions.
母体营养不良显著增加了后代患代谢和神经发育障碍的风险。母体营养不良的动物模型已经确定了成年后代在执行功能和奖励处理方面的行为变化。这些执行功能和基于奖励的行为变化可能共同导致与母体营养不良相关的代谢和神经发育障碍的发病机制。伴随着行为影响,母体营养不良改变了与控制执行功能和奖励的大脑通路中与奖励相关的分子和炎症信号的后代表达。神经免疫途径和这些特定脑回路中的小胶质细胞相互作用,无论是在早期发育还是在成年后期,都可能直接导致母体营养不良引起的行为表型。了解这些机制将有助于推进代谢和神经发育障碍的治疗策略,特别是非侵入性饮食补充干预措施。