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.
Strong parental bonds are critical for human development and mental health. We have the opportunity to take advantage of highly conserved neuronal circuits in laboratory mice to better understand the molecular and neural foundation of the positive and negative regulation of parenting. Results from this study will provide a more thorough characterization of the negative regulation of parenting, specifically behaviors characterized as infant-directed aggression.
