Adverse childhood experiences (ACEs) are traumatic events that can happen during the developmental stages of childhood, including abuse, neglect, and household dysfunction. Current literature highlights that many SGMs are at a higher risk of experiencing child abuse, including emotional, physical, and sexual abuse, compared to their heterosexual peers. This study explores how early exposure to ACE among sexual and gender minorities (SGMs) impacts on mental health impacts and the importance of trauma-informed care models and community-based practices that are responsive to the specific needs of these individuals. As these experiences have been linked to long-term effects on overall well-being. Specifically, this research explores the unique forms of trauma faced by SGM individuals during their childhood and includes various forms of household dysfunction. Participants were recruited using flyers posted on community boards around the Austin, Texas area and through social media. Directed individuals to an anonymous survey, which used a mixed-methods approach, the quantitative component includes structured, closed-ended questions, while the qualitative component includes open-ended questions allowing participants to elaborate on their experiences. By centering the voices of SGMs with lived experience of ACEs, we hope to inform trauma-informed care models and community-based practices that are responsive to the specific needs of these individuals. This study contributes to the existing body of knowledge by offering a more nuanced understanding of identity-based trauma and its lasting impact. Additionally, it provides valuable insight for shaping policy and social services that protect vulnerable youth from discrimination and emotional harm, particularly those related to gender and sexual identity.

Maternal experiences of childhood trauma are known to adversely affect mental health during pregnancy and may influence infant outcomes through biological and behavioral pathways. A growing body of research suggests that the effects of early adversity can be transmitted intergenerationally, increasing the risk of emotion dysregulation in offspring. Resilience, or the capacity to adapt in the face of hardship, has emerged as a protective factor that may buffer the impact of adverse childhood experiences (ACEs). The purpose of this study was to explore whether maternal resilience moderated the association between maternal adverse childhood experiences and infant emotion dysregulation at seven months postpartum. During their third trimester, participants (N = 123) completed the Connor-Davidson Resilience Scale (CD-RISC) and the Traumatic Experiences of Betrayal Across the Lifespan (TEBL) measure to assess resilience and ACEs. At seven months postpartum, participants completed the Infant Behavior Questionnaire – Very Short Form (IBQ-VSF) to assess infant emotion regulation. Contrary to hypotheses, maternal ACEs did not significantly predict infant emotion dysregulation (b = 0.07, p = .115), and resilience did not moderate the association between maternal ACEs and infant emotion dysregulation (b = 0.0001, p = .897). These results suggest that maternal childhood trauma does not directly translate to infant emotion regulation outcomes in early infancy. Future research should investigate additional protective factors, such as social support or parenting behaviors, which may influence early emotional development and further clarify the mechanisms of intergenerational trauma.

Children's psychopathology is an area that has recently become increasingly researched. However, the impact on adulthood has not been studied extensively. It has been found that 13 percent of children aged 3 to 17-years old experience a mental or behavioral health condition (CDC, 2025). Similarly, 50 percent of adult mental health disorders began before the age of 14, which shows a significant impact of childhood disorders on adulthood (Kessler et al., 2005). With work being a primary concern of adulthood, the impact of childhood disorders on work ethics specifically is an important variable to research. This study is therefore aimed at investigating the impact of childhood psychopathology on adults’ work ethic. The findings will add to the pool of research already out there on the effects of childhood disorders and increase the push to provide mental health treatment to the youth. Data will be collected through Survey Monkey software using a questionnaire developed by modifying other questionnaires as well as a demographic section. Participants will be adults 18 years or older recruited from the general population. Univariate Analysis of Variance will be conducted to examine the effects of demographics variables and childhood disorders on work ethic. Additional analysis, including correlations and regressions, will be conducted to examine the relationship between variables. The results will be presented at the conference, and the implications will be further discussed.

Synaptic specificity and synapse formation are fundamental to neural circuit function, yet the mechanisms governing synaptic partner selection remain poorly understood. Latrophilins (Lphns), a subset of adhesion G-protein coupled receptors (aGPCRs), mediate synaptic specificity and formation through transcellular interactions with presynaptic cell-adhesion molecules and GPCR signaling. While Lphns promote excitatory synapse formation in the hippocampus, their role in the striatum, which predominantly consists of dopamine D1 and D2 receptor-expressing medium spiny neurons (MSNs), remains elusive. D1 MSNs form the direct pathway, whereas D2 MSNs comprise the indirect pathway, establishing distinct neuronal circuits within the basal ganglia. Diverse glutaminergic inputs from cortex, thalamus, amygdala, and dopaminergic signals from substantia nigra and ventral tegmental area converge on MSNs. This enables the striatum to regulate motor movements, cognition, decision-making, and reward processing. However, the mechanisms by which these inputs are organized to regulate MSN activity are not yet understood. Our preliminary data reveal that conditional knockout (cKO) of Lphns in D2 MSNs leads to significant alterations in excitatory and inhibitory spontaneous postsynaptic currents and dramatically attenuates behavioral response to amphetamine. To further investigate, we will employ rabies virus-based retrograde tracing to map changes in presynaptic connectivity onto D2 MSNs in Lphn D2 cKO mice. Additionally, we use immunohistochemistry to assess synaptic puncta in Lphn D1 cKO mice, providing insight into synapse number and organization. Investigating how Lphns regulate synaptic inputs onto MSNs, our study aims to uncover fundamental mechanisms of striatal circuit assembly and inform potential therapeutic developments for disorders involving striatal dysfunction.