Motherhood, Oxytocin and the Medial Prefrontal Cortex

产后期伴随着荷尔蒙的剧烈变化，包括糖皮质激素的增加。 并降低雌激素水平。在处女啮齿动物中，高糖皮质激素和低雌激素水平 与树突结构减少和树突棘减少相关，树突棘是兴奋性突触的部位 内侧前额叶皮质(MPFC)。这种荷尔蒙环境也被证明具有负面影响。 由mPFC介导的行为，通过损害认知功能和增强焦虑。尽管已知 高糖皮质激素和低雌激素水平的有害影响，具有这种荷尔蒙特征的母亲表现出 减轻焦虑。此外，在K99阶段进行的研究表明，树突棘 母鼠mPFC的密度增加，这一效应与改善注意力和 行为灵活性，依赖于mPFC的功能。然而，保护母体的因素 来自潜在的产后荷尔蒙环境的mPFC仍不清楚。神经肽 催产素已被证明可以缓冲压力荷尔蒙对大脑和行为的影响，并可能在 在孕期保护mPFC的结构和功能。为了研究这一点，催产素的操作 受体、认知、焦虑和母体行为分析以及结构可塑性的测量将是 受雇的。这些研究的结果将告诉我们与以下相关的神经和行为变化 以及催产素在这些变化中可能扮演的角色。这部作品是独立的 K99/R00奖的一部分，并将为专注于阐明 大脑弹性的机制。

The postpartum period is accompanied by dramatic clianges in hormones, including increased glucocorticoid and decreased estrogen levels. In virgin rodents, high glucocorticoid and low estrogen levels have been associated with diminished dendritic architecture and fewer dendritic spines, sites of excitatory synapses, in the medial prefrontal cortex (mPFC). This hormonal environment has also been shown to negatively impact behaviors mediated by the mPFC, by impairing cognitive function and enhancing anxiety. Despite the known detrimental effects of high glucocorticoid and low estrogen levels, mothers with this hormonal profile exhibit attenuated anxiety. In addition, research conducted during the K99 phase has shown that dendritic spine density is increased in the mPFC of mother rats and that this effect coincides with improved attention and behavioral flexibility, functions that depend on the mPFC. However, the factors that shield the maternal mPFC from the potentially damaging postpartum hormonal milieu remain unknown. The neuropeptide oxytocin has been shown to buffer stress hormone effects on the brain and behavior and may play a role in protecting mPFC structure and function during motherhood. To investigate this, manipulations of oxytocin receptors, cognitive, anxiety, and maternal behavioral assays and measures of structural plasticity will be employed. The results of these studies will inform us ofthe neural and behavioral alterations associated with motherhood and the role that oxytocin may play in these changes. This work serves as the independent portion of the K99/R00 award and will provide the foundation for a research program focused on elucidating the mechanisms of brain resilience.