Preexisting risk-avoidance and enhanced alcohol relief are driven by imbalance of the striatal dopamine receptors in mice

Miriam E. Bocarsly (), Marlisa J. Shaw, Emilya Ventriglia, Lucy G. Anderson, Hannah C. Goldbach, Catherine E. Teresi, Marilyn Bravo, Roland Bock, Patrick Hong, Han Bin Kwon, Imran M. Khawaja, Rishi Raman, Erin M. Murray, Jordi Bonaventura, Dennis A. Burke, Michael Michaelides and Veronica A. Alvarez ()
Additional contact information
Miriam E. Bocarsly: NIH
Marlisa J. Shaw: NIH
Emilya Ventriglia: NIH
Lucy G. Anderson: NIH
Hannah C. Goldbach: NIH
Catherine E. Teresi: NIH
Marilyn Bravo: NIH
Roland Bock: NIH
Patrick Hong: Rutgers New Jersey Medical School
Han Bin Kwon: NIH
Imran M. Khawaja: Rutgers New Jersey Medical School
Rishi Raman: Rutgers New Jersey Medical School
Erin M. Murray: NIH
Jordi Bonaventura: NIH
Dennis A. Burke: NIH
Michael Michaelides: NIH
Veronica A. Alvarez: NIH

Nature Communications, 2024, vol. 15, issue 1, 1-17

Abstract: Abstract Alcohol use disorder (AUD) is frequently comorbid with anxiety disorders, yet whether alcohol abuse precedes or follows the expression of anxiety remains unclear. Rodents offer control over the first drink, an advantage when testing the causal link between anxiety and AUD. Here, we utilized a risk-avoidance task to determine anxiety-like behaviors before and after alcohol exposure. We found that alcohol’s anxiolytic efficacy varied among inbred mice and mice with high risk-avoidance showed heightened alcohol relief. While dopamine D1 receptors in the striatum are required for alcohol’s relief, their levels alone were not correlated with relief. Rather, the ratio between striatal D1 and D2 receptors was a determinant factor for risk-avoidance and alcohol relief. We show that increasing striatal D1 to D2 receptor ratio was sufficient to promote risk-avoidance and enhance alcohol relief, even at initial exposure. Mice with high D1 to D2 receptor ratio were more prone to continue drinking despite adverse effects, a hallmark of AUD. These findings suggest that an anxiety phenotype may be a predisposing factor for AUD.

Date: 2024
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DOI: 10.1038/s41467-024-53414-y

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