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Basolateral amygdala neuropeptide Y system modulates binge ethanol consumption

Neuropsychopharmacology volume 49, pages 690–698 (2024)Cite this article

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Abstract

Neuropeptide Y (NPY) signaling regulation of corticolimbic communication is known to modulate binge-like ethanol consumption in rodents. In this work we sought to assess the impact of intra-BLA NPY system modulation on binge-like ethanol intake and to assess the role of the NPY1R+ projection from the BLA to the mPFC in this behavior. We used “drinking-in-the-dark” (DID) procedures in C57BL6J mice to address these questions. First, the impact of intra-BLA administration of NPY on binge-like ethanol intake was assessed. Next, the impact of repeated cycles of DID intake on NPY1R expression in the BLA was assessed with use of immunohistochemistry (IHC). Finally, chemogenetic inhibition of BLA→mPFC NPY1R+ projections was assessed to determine if limbic communication with the mPFC was specifically involved in binge-like ethanol intake. Importantly, as both the BLA and NPY system are sexually dimorphic, both sexes were assessed in these studies. Intra-BLA NPY dose-dependently decreased binge-like ethanol intake in males only. Repeated DID reduced NPY1R expression in the BLA of both sexes. Silencing of BLA→mPFC NPY1R+ neurons significantly reduced binge-like ethanol intake in both sexes in a dose-dependent manner. We provide novel evidence that (1) intra-BLA NPY reduces binge-like ethanol intake in males; (2) binge-like ethanol intake reduces NPY1R levels in the BLA; and (3) chemogenetic inhibition of BLA→mPFC NPY1R+ neurons blunts binge-like drinking in male and female mice. These observations provide the first direct evidence that NPY signaling in the BLA, and specifically BLA communication with the mPFC, modulates binge-like ethanol consumption.

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Fig. 1: Intra-BLA NPY dose dependently decreases binge-like ethanol intake in male mice.
Fig. 2: Intra-BLA NPY does not impact sucrose intake or general locomotion.
Fig. 3: Three cycles of ethanol DID decreases NPY1R expression in the BLA.
Fig. 4: Chemogenetic inhibition of BLA → mPFC NPY1R+ projections inhibits binge-like ethanol intake in a dose-dependent manner.
Fig. 5: Schematic representation of the neurocircuitry under investigation and hypothetical mechanisms of action.

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Acknowledgements

Special thanks to Rhiannon Thomas, MS, for technical assistance and feedback.

Funding

This work was supported by NIH grants AA022048, AA013573, AA025809, F32AA025811, and K99AA028268.

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  1. Department of Psychology & Neuroscience, The University of North Carolina, Chapel Hill, NC, 27599-3270, USA

    Stacey L. Robinson, Sophie C. Bendrath, Elizabeth M. Yates & Todd E. Thiele

  2. Bowles Center for Alcohol Studies, The University of North Carolina, Chapel Hill, NC, 27599-7178, USA

    Stacey L. Robinson, Sophie C. Bendrath & Todd E. Thiele

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SLR: conception and design of the work; acquisition, analysis, and interpretation of data; and drafting and revising of manuscript. SCB: design of work; acquisition of data; manuscript review. EMY: acquisition of data. TET: conception and design of the work; revising of manuscript; final approval of the version to be published.

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The authors declare no competing financial interests. Dr. Thiele owns shares of Glauser Life Sciences, a company focusing on the development of therapeutics for mental health disorders. The work that is presented in this paper is not directly related to the scientific aims of Glauser Life Sciences.

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Robinson, S.L., Bendrath, S.C., Yates, E.M. et al. Basolateral amygdala neuropeptide Y system modulates binge ethanol consumption. Neuropsychopharmacol. 49, 690–698 (2024). https://doi.org/10.1038/s41386-023-01742-w

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