# Delineating the epigenetic and neural mechanisms by which early life scarcity alters motivated behavior

> **NIH NIH R01** · TEMPLE UNIV OF THE COMMONWEALTH · 2022 · $643,242

## Abstract

PROJECT SUMMARY
Early life experiences can have profound and long-lasting consequences on health trajectories. Social inequities,
such as those caused by low resources, have been identified as important factors that influence the development
of psychiatric illnesses, including substance use disorders (SUD). In this proposal, a rat model of early life
scarcity will be combined with behavioral paradigms of substance abuse to better understand the neural and
molecular mechanisms that influence reward processing in individuals who experienced adversity early in life.
Each brain region contains highly heterogenous cell populations that include different neuronal subtypes as well
as glia. Accounting for the diversity and differences in cell types is essential to improving our understanding of
the impact of inequities on the brain and on motivated behavior. In this proposal, the influence of early life scarcity
on adult reward processing and motivation will be characterized in male and female rats using state-of-the-art
behavioral approaches where rats are tested for their motivation to earn drug (opioid) or natural (social and
sucrose) rewards. Our preliminary data indicate sex- and reinforcer-specific effects of early scarcity. This work
will be expanded here, and in some of the experiments, rats will choose between two available reinforcers. Given
that interventions for SUD involve social reinforcers, these results could have profound implications for the
prevention and treatment of SUD in populations who experience socioeconomic inequality. To better identify
factors that mediate the effects of early scarcity on motivated behavior, we will delineate molecular changes in
the nucleus accumbens—a central hub in the brain that is critical for motivated and reward-related behaviors—
and causally link them to behavior. To this end, we will perform cell-type specific assays of gene expression and
chromatin remodeling, an epigenetic process that regulates the expression of genes. Lastly, the proposal will
examine the impact of early life scarcity on the electrophysiological properties of two major neuron subtypes in
the nucleus accumbens, delineating cell type-specific physiological changes induced by altering the early
environment. Collectively, this proposal leverages cutting-edge behavioral, molecular, and physiological
approaches to provide a better understanding of the neurochemical and intracellular pathways affected by early
life scarcity that drive changes in motivated behavior. Importantly, the proposed experiments will determine sex-
and cell-type specific mechanisms by which early life scarcity alters the substance use trajectory, identifying
potential targets for improving therapeutics and prevention of SUDs.

## Key facts

- **NIH application ID:** 10508379
- **Project number:** 1R01DA056534-01
- **Recipient organization:** TEMPLE UNIV OF THE COMMONWEALTH
- **Principal Investigator:** Debra A Bangasser
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $643,242
- **Award type:** 1
- **Project period:** 2022-07-01 → 2027-04-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10508379

## Citation

> US National Institutes of Health, RePORTER application 10508379, Delineating the epigenetic and neural mechanisms by which early life scarcity alters motivated behavior (1R01DA056534-01). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10508379. Licensed CC0.

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