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Error-related signaling in nucleus accumbens D2 receptor-expressing neurons guides inhibition-based choice behavior in mice

Author

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  • Tadaaki Nishioka

    (Osaka University
    Icahn School of Medicine at Mount Sinai)

  • Suthinee Attachaipanich

    (Osaka University)

  • Kosuke Hamaguchi

    (Kyoto University)

  • Michael Lazarus

    (University of Tsukuba)

  • Alban Kerchove d’Exaerde

    (Université Libre de Bruxelles)

  • Tom Macpherson

    (Osaka University)

  • Takatoshi Hikida

    (Osaka University)

Abstract

Learned associations between environmental cues and the outcomes they predict (cue-outcome associations) play a major role in behavioral control, guiding not only which responses we should perform, but also which we should inhibit, in order to achieve a specific goal. The encoding of such cue-outcome associations, as well as the performance of cue-guided choice behavior, is thought to involve dopamine D1 and D2 receptor-expressing medium spiny neurons (D1-/D2-MSNs) of the nucleus accumbens (NAc). Here, using a visual discrimination task in male mice, we assessed the role of NAc D1-/D2-MSNs in cue-guided inhibition of inappropriate responding. Cell-type specific neuronal silencing and in-vivo imaging revealed NAc D2-MSNs to contribute to inhibiting behavioral responses, with activation of NAc D2-MSNs following response errors playing an important role in optimizing future choice behavior. Our findings indicate that error-signaling by NAc D2-MSNs contributes to the ability to use environmental cues to inhibit inappropriate behavior.

Suggested Citation

  • Tadaaki Nishioka & Suthinee Attachaipanich & Kosuke Hamaguchi & Michael Lazarus & Alban Kerchove d’Exaerde & Tom Macpherson & Takatoshi Hikida, 2023. "Error-related signaling in nucleus accumbens D2 receptor-expressing neurons guides inhibition-based choice behavior in mice," Nature Communications, Nature, vol. 14(1), pages 1-15, December.
  • Handle: RePEc:nat:natcom:v:14:y:2023:i:1:d:10.1038_s41467-023-38025-3
    DOI: 10.1038/s41467-023-38025-3
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