Maturation of Social and Non-Social Reward Processing in the Adolescent Amygdala and Orbitofrontal Cortex

NIH RePORTER · MH · R01 · $572,672 · view on reporter.nih.gov ↗

Abstract

ABSTRACT Adolescence is a time of substantial development attributed to the maturation of brain circuits that underlie the acquisition of new cognitive, emotional, and social skills. It is also a time of maximum vulnerability for mental disorders. In the past decade, the incidence of anxiety, depression, and suicide increased by ~60% in adolescents, remarkably more in females than in males. The social isolation during the COVID-19 pandemic added to the severity of the national and international statistics. To fully address the current youth mental health crisis, we need to understand how and why the dramatic reorganization of the adolescent brain contributes to the increased vulnerability to mental disorders. The studies proposed here rest on the assumption that the remodeling of the reward circuits of the brain creates the shared foundation of cognitive, affective, and social maturation during adolescence. Our multifaceted project addresses foundational gaps in our knowledge on how reward-driven motivational states inform adolescent behaviors such as risk-taking, pleasure-seeking, impulsivity, and a range of emotional responses to challenges of the social environment. We designed a within-subject, longitudinal study that spans the 2.5 - 3-year duration of adolescence in non-human primates. During this period, we will obtain repeated samplings of neurophysiological data recorded from the amygdala and orbitofrontal cortex in the context of the same behavioral tasks. In parallel, we will longitudinally monitor morphometric and microstructural changes in the gray and white matter of the brain through serial MRI scans, complemented by physical and hormonal measures of pubertal maturation. The three specific aims address the neural basis of three different aspects of reward processing in the subcircuit of the amygdala and orbitofrontal cortex. First, we will use a delay discounting task to determine the cellular and circuit level changes that underlie the increasing tole

Key facts

NIH application ID
11235155
Project number
5R01MH135267-03
Recipient
UNIVERSITY OF ARIZONA
Principal Investigator
Steve W. C. Chang; Katalin M Gothard
Activity code
R01
Funding institute
MH
Fiscal year
2026
Award amount
$572,672
Award type
5
Project period
2024-02-20T00:00:00 → 2028-11-30T00:00:00