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Med Sci (Paris). 2015 May;31(5):546-50. doi: 10.1051/medsci/20153105017. Epub 2015 Jun 9.

[Depression and addiction comorbidity: towards a common molecular target?].

[Article in French]

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Département de physiologie, institut de génomique fonctionnelle, Inserm U661, CNRS UMR5203, 141, rue de la Cardonille, 34090 Montpellier, France.
Département de chirurgie neurologique, Weill Cornell Medical College, 1300 York Avenue, New York, 10021 NY, États-Unis.


The comorbidity of depression and cocaine addiction suggests shared mechanisms and anatomical pathways. Specifically, the limbic structures, such as the nucleus accumbens (NAc), play a crucial role in both disorders. P11 (S100A10) is a promising target for manipulating depression and addiction in mice. We summarized the recent genetic and viral strategies used to determine how the titration of p11 levels within the NAc affects hedonic behavior and cocaine reward learning in mice. In particular, p11 in the ChAT+ cells or DRD1+ MSN of the NAc, controls depressive-like behavior or cocaine reward, respectively. Treatments to counter maladaptation of p11 levels in the NAc could provide novel therapeutic opportunities for depression and cocaine addiction in humans.

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