The role of the amygdalohippocampal area in infant-directed aggression

项目摘要/摘要 养育对婴儿的生存至关重要。然而，这些行为在不同物种之间高度保守。 许多作为父母的动物也表现出直接反对幼崽生存的行为。这些行为 被归类为针对婴儿的攻击行为，通常会导致婴儿受伤或死亡。例如, 在实验室小鼠中，处女雄性自发地杀婴，而处女雌性通常是母性的。 这种现象最有趣的方面是，处女雄性在与一只雄性雄性交配后成为父亲 女性。这一行为转换表明，构成婴儿定向攻击行为的神经回路可能是 受社会经验的控制，比如交配。关于父母教养的积极控制，人们知道得很多，而 婴儿定向攻击的神经回路还没有得到很好的研究。穹隆周围区的Urocortin-3神经元 (PeFAUcn3)最近被发现对婴儿忽视和攻击是必要的。PeFAUcn3纤维项目 最密集的是杏仁核海马区(AHI)，这是一个功能不明确的脑区。光遗传 刺激AHI中的PeFAUcn3终末促进处女的婴儿定向攻击，而 抑制可以消除男性的这种行为。在所研究的PeFAUcn3投射中，AHI刺激导致 对婴儿的攻击性有最显著的影响。这些结果表明，AHI在功能上是一种 在控制婴儿定向攻击的环路中有显著的大脑区域。我怀疑反应神经 AHI人群表达UCN3‘S主要受体促肾上腺皮质激素释放因子受体2(CRFR2)。 因此，我假设ahi中的一部分神经元对于婴儿导向是必不可少的。 攻击性。我的中心假设将在两个具体目标中得到检验：(1)表征分子同一性 AHI神经元参与婴儿定向攻击，以及(2)确定CRFR2神经元在AHI中的功能 在婴儿导向的行为中。这项研究的结果将提供对分子组成的洞察 在婴儿定向攻击期间活跃的AHI神经元，目前发现与 这是一个功能不明确的大脑区域。总体而言，这项工作将增加我们对婴儿的了解- 定向攻击性和父母教养的规范。

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.