Abstract
The brain’s reward-processing circuitry remains sensitive to experience throughout early life and into adulthood, allowing individuals to adapt to their unique environments. Adverse experiences early in life can increase vulnerability to substance use disorders, likely through alterations to this circuitry. Yet, the precise neurobiological mechanisms by which early life adversity acts are incompletely characterized. In this study, we used a limited bedding and nesting (LBN) paradigm as a translationally relevant model of early life adversity in isogenic C57BL/6J mice. After LBN-rearing, we assessed the lasting behavioral and neurobiological impacts of this experience in adulthood. In robust sample sizes, our results validated previous findings of increased risk avoidance, enhanced acute locomotor response to alcohol, and greater voluntary alcohol drinking in socially-housed LBN-reared mice, especially males. Further, using autoradiography, we found LBN-reared mice had increased striatal D1-like receptor binding, skewing D1- to D2-like receptor balance relative to cross-fostered controls. However, after voluntary alcohol drinking, we found a strong downregulation in D1-like, and some D2-like, receptor binding, negating pre-existing differences in striatal dopamine receptor binding. We posit that via both transcriptional and post-transcriptional mechanisms, LBN-rearing upregulates striatal D1-receptor density and alters risk avoidance and acute alcohol stimulation to promote alcohol drinking among adversity-exposed mice. Together, these findings reveal specific neurobiological mechanisms that promote alcohol consumption following early life adversity and suggest complex interactions between early life adversity, sex-related factors, and dopamine receptor regulation in contributing to alcohol use disorder (AUD) vulnerability.
Data availability
All data and code are accessible on Mendeley. Reserved: https://doi.org/10.17632/5ygmcc6cm4.2.
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Acknowledgements
We would like to thank the NIMH IRP Rodent Behavioral Core for their help with behavioral testing and Drs. Miriam Bocarsly and Yan Leng for their technical advice. Additionally, we would like to thank Mikal Armstrong, our former HI-STEP 2.0 intern, for her help running IntelliCage experiments. The contributions of the NIH authors were made as part of their official duties as NIH federal employees, are in compliance with agency policy requirements, and are considered Works of the United States Government. However, the findings and conclusions presented in this paper are those of the authors and do not necessarily reflect the views of the NIH or the U.S. Department of Health and Human Services.
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This work was supported by funding from the NIH Intramural Research Program of the National Institutes of Health to V.A.A. (ZIA AA000421; ZIA MH002987) and to M.M. (ZIA DA000069).
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Conceptualized by LGA, VAA, RB, and MM. All experimentation except autoradiography conducted by LGA. Autoradiography conducted by AET. Technical support by RB. Formal analysis by LGA, AET, and RB. Writing and figure design by LGA. Review and editing by all authors. Funding acquisition by VAA and MM.
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Anderson, L.G., Tischer, A.E., Bock, R. et al. Early life adversity increases striatal dopamine D1 receptor density and promotes social alcohol drinking in mice, especially males. Transl Psychiatry (2026). https://doi.org/10.1038/s41398-026-04033-2
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DOI: https://doi.org/10.1038/s41398-026-04033-2