Early life adversity (ELA) is a prevalent experience in young populations worldwide and can come in many forms, including limited access to resources as in many low socio-economic status households. ELA in humans has been linked to a variety of negative psychiatric outcomes including increased risk for psychiatric disorders such as schizophrenia, major depressive disorder (MDD), post-traumatic stress disorder (PTSD) and substance use disorder (SUD). One characteristic that these disorders share is a disruption in motivational processes. Motivation is largely regulated by the mesocorticolimbic dopamine (DA) system but is also modulated by other brain regions including the medial preoptic area (mPOA) and is crucial for processing of natural rewards such as sexual reproduction. This circuitry is sensitive to estrogenic and androgenic signaling in both males and females. Interestingly, estrogens and androgens can be modulated by the experience of ELA, pointing to gonadal hormones as a potential mediator for the impact of ELA on motivation and risk for psychiatric disorders. In the first set of experiments presented here, we characterize the limited bedding and nesting model (LBN) of early life adversity in rodents, in which rat dams and their pups are housed in a limited resource environment from postnatal day (PND) 2 through 9. LBN dams exhibited less self-care behaviors and more pup-directed behaviors, including grooming and nursing, compared to control dams. This type of maternal care is not characteristic of healthy rat dam behavior and may represent a compensatory mechanism to combat the lack of resources. However, LBN-raised pups still exhibit developmental alterations, notably a decrease in body weight that persisted into adulthood and an increase in adult plasma estradiol levels specifically in males. We build on these findings in the second set of experiments, which explores whether changes in development and gonadal hormones may also impact male reproductive behavior. We found that LBN males have a shorter latency to engage in sex behaviors at earlier timepoints in the sex assay compared to controls, suggesting an enhancement in the acquisition of this repertoire of behaviors. This enhancement in behavior was accompanied by highly sex-specific changes in gene transcription in the mPOA which underlies reproductive behaviors. The identification of genes and signaling pathways that are altered by LBN in the male mPOA lays the groundwork for future studies investigating the mechanisms by which ELA alters reproductive behaviors and underlying motivational processes. / Psychology

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