# Parallel maturation of social behaviors and amygdala circuits > **NIH NIH R01** · ROSALIND FRANKLIN UNIV OF MEDICINE & SCI · 2024 · $535,696 ## Abstract Adolescence is a critical window for social maturation. Harmful experiences during adolescence can produce life-long social impairments, partly by impacting key brain regions involved in social function, such as the amygdala. The long-term goal of our research is to understand how experience during development shapes the amygdala and its connections, and how their dysfunction produces social impairments. Social motivation drives engagement in social behaviors, but there is a homeostatic balance that is sensitive to social deprivation and satiety, and social behaviors need to reflect this balance. In our prior project period, we found that medial amygdala (MeA) and basolateral amygdala (BLA) have complementary roles in social behaviors and different sensitivities to factors that temper social motivation. We also demonstrated differences between adult and adolescent social motivation, and their sensitivity to social change. But there is a gap in our understanding of the synaptic and molecular changes that adjust social motivation over short behavioral timescales and larger timescales between adolescence and adulthood. The prefrontal cortex (PFC) sends excitatory glutamatergic projections to BLA, matures during adolescence, and has a key role in regulation of many social behaviors. Our short-term goal is to uncover the synaptic and microcircuit changes at the PFC-BLA interface that regulate social motivation, and how this matures during adolescence. Fast glutamatergic synaptic responses in the BLA are predominantly driven by AMPA receptors (AMPAR), whose impact depends on the subunit composition. Based on the prior project period and preliminary data, we propose that there are functional shifts in relative AMPAR subunit composition at PFC-BLA synapses to BLA output neurons, and to BLA GABAergic interneurons that regulate output neurons. These contribute to a shift in social motivation during adolescence, and to rapid shifts during social deprivation and satiety. We will test the hypotheses that during transition from adolescence to adulthood there is a functional redistribution of AMPAR subunits so that PFC glutamatergic inputs to BLA GABAergic interneurons gain relative strength compared to BLA output neurons, and changes in social motivation rapidly change AMPAR subunit composition at PFC-BLA synapses to permit an appropriate adaptation in social behavior. The Aims of this project are to determine (1) cellular and synaptic elements in BLA that contribute to emergence of a mature PFC-BLA impact, (2) the role of AMPAR at PFC-BLA synapses in adapting to social motivation changes, and (3) the functional impact of PFC inputs on BLA encoding of social cues during changes in social motivation. This project is significant because it will delineate a synaptic mechanism for modulation of social motivation, and how this matures into adulthood. This will yield exciting new perspectives about parallel development of social regulation and PFC-BLA circuits, and ... ## Key facts - **NIH application ID:** 11049532 - **Project number:** 2R01MH118237-06A1 - **Recipient organization:** ROSALIND FRANKLIN UNIV OF MEDICINE & SCI - **Principal Investigator:** Jeremy E Rosenkranz - **Activity code:** R01 (R01, R21, SBIR, etc.) - **Funding institute:** NIH - **Fiscal year:** 2024 - **Award amount:** $535,696 - **Award type:** 2 - **Project period:** 2019-03-01 → 2029-06-30 ## Primary source NIH RePORTER: https://reporter.nih.gov/project-details/11049532 ## Citation > US National Institutes of Health, RePORTER application 11049532, Parallel maturation of social behaviors and amygdala circuits (2R01MH118237-06A1). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/11049532. Licensed CC0. --- *[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*