The role of the amygdalohippocampal area in infant-directed aggression

项目总结/摘要 养育对婴儿的生存至关重要。然而，这些行为在物种之间是高度保守的。 许多动物的父母也表现出直接反对年轻人生存的行为。这些行为 被归类为针对婴儿的攻击，往往导致婴儿受伤或死亡。比如说， 在实验室小鼠中，未交配的雄性小鼠自发地杀雄激素，而未交配的雌性小鼠通常是母性的。 这一现象最有趣的方面是，处女男性成为父系交配后， 女性这种行为转换表明，婴儿定向攻击的神经回路可能是 受社会经验的影响比如交配关于父母的积极控制已经知道很多， 婴儿主导的攻击行为的神经回路还没有得到很好的研究。穹窿周围区的Urocortin-3神经元 （PeFAUcn 3）最近被发现是必要的婴儿忽视和侵略。PeFAUcn 3纤维项目 最密集的是杏仁海马区（AHi），一个功能上没有特征的大脑区域。光遗传 刺激AHi中的PeFAUcn 3终末有助于处女雌性的婴儿定向攻击， 抑制消除了雄性的这种行为。在所研究的PeFAUcn 3投射中，AHi刺激导致 对婴儿的攻击性影响最明显。这些结果表明，AHi是一种功能性的 控制婴儿攻击性的重要脑区我怀疑这个反应神经元 AHi中的细胞群表达Ucn 3的主要受体，促肾上腺皮质激素释放因子受体2（CRFR 2）。 因此，我假设AHi中的一个神经元子集对于婴儿定向的 侵略我的中心假设将在两个特定的目标进行测试：（1）表征的分子身份， AHi神经元参与婴儿定向攻击，以及（2）确定AHi神经元中CRFR 2神经元的功能 在婴儿的行为中。这项研究的结果将提供深入了解的分子组成， AHi神经元在婴儿定向攻击过程中活跃，目前确定了行为相关性， 这个功能上没有特征的大脑区域。总的来说，这项工作将增加我们对婴儿的了解- 直接攻击和父母的监管。

Project Summary/Abstract Parenting is essential to the survival of infants. These behaviors are highly conserved across species, however many animals that parent also exhibit behaviors that directly oppose the survival of young. These behaviors are categorized as infant-directed aggression and often result in the injury or death of an infant. For instance, in laboratory mice, virgin males are spontaneously infanticidal whereas virgin females are typically maternal. The most interesting aspect of this phenomenon is that virgin males become paternal after mating with a female. This behavioral switch suggests that neural circuits that underlie infant-directed aggression may be regulated by social experience, like mating. Much is known regarding the positive control of parenting, while the neural circuitry of infant-directed aggression is not well studied. Urocortin-3 neurons of the perifornical area (PeFAUcn3) have recently been found necessary for infant neglect and aggression. The PeFAUcn3 fibers project most densely to the amygdalohippocampal area (AHi), a functionally uncharacterized brain region. Optogenetic stimulation of PeFAUcn3 terminals in the AHi facilitates infant-directed aggression in virgin females whereas inhibition abolishes this behavior in males. Of the studied PeFAUcn3 projections, AHi stimulation resulted in the most pronounced effects on infant-directed aggression. These results suggest that the AHi is a functionally significant brain area in circuits governing infant-directed aggression. I suspect that the responding neural population in the AHi expresses Ucn3’s primary receptor, corticotropin releasing factor receptor 2 (CRFR2). Therefore, I hypothesize that a subset of neurons in the AHi are essential for infant-directed aggression. My central hypothesis will be tested in two specific aims: (1) characterize the molecular identity of AHi neurons involved in infant-directed aggression, and (2) identify the function of CRFR2 neurons in the AHi during infant-directed behavior. Results from this study will provide insight into the molecular composition of AHi neurons that are active during infant-directed aggression and currently identify a behavioral relevance for this functionally uncharacterized brain area. Overall, this work will increase our understanding of the infant- directed aggression and the regulation of parenting.