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Updated: Apr 11, 2026

Investigating Drivers of Antireward in Addiction Behavior with Anatomically Specific Single-Cell Gene Expression Methods
Published on: August 4, 2022
[Depression and addiction comorbidity: towards a common molecular target?]
Margarita Arango-Lievano1, Michael G Kaplitt2
1Département de physiologie, institut de génomique fonctionnelle, Inserm U661, CNRS UMR5203, 141, rue de la Cardonille, 34090 Montpellier, France.
The protein P11 (S100A10) in the nucleus accumbens (NAc) influences depression and cocaine addiction. Targeting P11 levels in specific NAc cells offers potential new therapies for these co-occurring disorders.
Area of Science:
- Neuroscience
- Molecular Biology
- Addiction Research
Context:
- Depression and cocaine addiction frequently co-occur, indicating shared underlying biological mechanisms.
- The nucleus accumbens (NAc), a key limbic structure, is implicated in the pathophysiology of both disorders.
- P11 (S100A10) has emerged as a significant molecular target for modulating behaviors associated with depression and addiction.
Purpose:
- To review genetic and viral strategies for investigating the role of P11 levels in the NAc.
- To elucidate how modulating P11 in specific NAc cell populations affects hedonic behavior and cocaine reward learning in mice.
Summary:
- P11 levels within the NAc are critical for regulating hedonic behavior and cocaine reward.
- Specifically, P11 within ChAT+ cells in the NAc controls depressive-like behaviors.
- P11 within DRD1+ medium spiny neurons (MSNs) of the NAc modulates cocaine reward learning.
Impact:
- Understanding P11's role in the NAc provides insights into the neurobiological links between depression and cocaine addiction.
- Therapeutic strategies targeting P11 maladaptation in the NAc may offer novel treatment avenues for comorbid depression and cocaine addiction.
- This research highlights P11 as a potential therapeutic target for complex psychiatric disorders.
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