Motherhood, Oxytocin and the Medial Prefrontal Cortex

产后期间伴随着激素的急剧变化，包括糖皮质激素的增加 雌激素水平下降在未交配过的啮齿类动物中，高糖皮质激素和低雌激素水平一直是 与减少树突结构和更少的树突棘，兴奋性突触的网站， 内侧前额叶皮层（mPFC）。这种荷尔蒙环境也被证明会对 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，具有这种激素特征的母亲表现出 减轻焦虑此外，在K99阶段进行的研究表明，树突棘 密度增加，在mPFC的母鼠，这种影响与改善注意力， 行为灵活性，依赖于mPFC的功能。然而，保护产妇的因素 来自潜在有害的产后激素环境的mPFC仍然未知。神经肽 催产素已被证明可以缓冲压力激素对大脑和行为的影响， 在母亲期间保护mPFC结构和功能。为了研究这个问题， 受体，认知，焦虑和母体行为测定和结构可塑性的措施将是 就业。这些研究的结果将告诉我们与神经和行为改变相关的 母性和催产素在这些变化中可能发挥的作用。这项工作作为独立的 K99/R 00奖的一部分，并将提供一个研究计划的基础，重点是阐明 大脑恢复力的机制

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.