# NIH grant: Social experience guides BMA mediated social development (1R01MH141161-01A1) — retained record

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[original source ↗](https://reporter.nih.gov/project-details/1R01MH141161-01A1)

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NIH grant 1R01MH141161-01A1: Social experience guides BMA mediated social development
Institute: {'code': 'MH', 'abbreviation': 'NIMH', 'name': 'National Institute of Mental Health', 'admin_org_id': '12500050', 'admin_funding_url': ''}. PI: Nicole Christine Ferrara. Award: $465301.
Start: 2026-07-25T00:00:00.
PROJECT SUMMARY/ABSTRACT
Social experiences are indispensable for mental health, and this is particularly important in younger populations
where there is a developmental need for peer-peer social interactions. Atypical social experiences in the form of
social isolation or deprivation became common during the COVID19 pandemic and have been particularly
harmful for adolescent mental health. This can be seen with impaired age-specific social behaviors, like play in
adolescent rats and investigation in adult rats. The poor social opportunity that arises from social deprivation
alters brain function that contributes to adolescent vulnerabilities to social perturbations. The amygdala is a
candidate brain region to investigate the impact of social deprivation on social development, as it is important for
regulating social behavior and is sensitive to atypical social experiences. Adolescent amygdala maturation is
epitomized by increases in inhibitory parvalbumin (PV) GABAergic tone and in activity evoked by the infralimbic
region of the medial prefrontal cortex (IL). The adult basomedial amygdala (BMA) in particular receives dense
inputs from the IL and is regulated by GABAergic neurons. Further, the adult BMA dynamically responds to social
stimuli and is unique in that its activity directly correlates to the degree of social interaction. Our preliminary data
show that BMA principal neuron activity regulates adolescent and adult social engagement. Within the BMA, we
have identified IL inputs as a source of BMA principal neuron activation. This IL-evoked principal neuron
activation is greater adolescents relative to adults, and the age-dependent reduction in IL-driven excitation is
regulated by inhibitory GABAergic neurons in adults. However, it is unclear how social deprivation compromises
unique developmental features of the BMA to subsequently impair social development. Our goal is to understand
the initial effects of adolescent and adult social deprivation on BMA-driven changes in social behavior, as these
initial changes will identify the adolescent-specific vulnerabilities when contrasted with adults. Our aims address
a novel central hypothesis that social deprivation shapes BMA activity through reductions in principal neuron
activity driven by the IL at both ages and reduction of PV activity in adults. This social deprivation-driven change
to BMA activity impairs social interaction across ages. Our central hypothesis will be tested in three specific aims
quantifying the contribution of excitation (Aim 1), PV activity (Aim 2), and the ILBMA pathway (Aim 3) to adult
and adolescent social behavior and how this is neural circuitry is impacted by social deprivation. Each aim will
use a combination of in vitro electrophysiology to mechanistically quantify BMA maturation, fiber photometry for
functional changes in BMA activity time-locked to social investigation, and chemogenetics to understand the
BMA regulation of adolescent and adult social behavior. The results from the proposed project are expected to
create a novel framework through which social deprivation shapes BMA activation underlying adolescent and
adult social dysfunction. This will identify distinguishing factors between ages that may contribute to age-specific
mechanisms of social abnormalities and adolescent vulnerability to social perturbations.
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