ArticleTranslational psychiatry2026
Chemogenetic modulation of the prelimbic cortex to the nucleus accumbens core pathway reduces cocaine-induced increase of risk preference.
Article in Translational psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Decision-making impairments are a core symptom of several psychiatric disorders, including gambling and substance use disorders (SUD). These disorders frequently co-occur, suggesting shared neurobiological mechanisms underlying dysfunctional decision-making. We previously demonstrated that chronic cocaine exposure increases risk preference in a rat gambling task (rGT). Given that the prelimbic cortex (PrL) to the nucleus accumbens (NAc) core pathway plays a crucial role in regulating risk-based decision-making, we further explored how chemogenetic modulation of this pathway alters cocaine-induced increase in risky decision-making in the rGT. Notably, activation of Gi, but not Gq, designer receptors exclusively activated by designer drugs (DREADD) in the PrL attenuated the cocaine-induced increase of risk preference in risk-averse rats, while simultaneously reducing cocaine-induced attentional deficits measured by task omissions. Subsequent molecular analyses revealed that cocaine significantly induced changes in the expression levels of calcium channel alpha 1 C subunit (CaV1.2) and in the ratio of phosphorylation at serine 97 of total dopamine- and cAMP-regulated phosphoprotein, 32 kDa (DARPP-32) in the PrL region of these rats, which returned to basal levels with concurrent Gi-DREADD activation. No significant behavioral or molecular changes were observed in risk-seeking rats. These results suggest that modulating the PrL-NAc core pathway can selectively control risk-based decision-making behavior and attentional processes affected by cocaine exposure, offering therapeutic potential for addressing decision-making impairments in dual diagnoses of gambling and SUD.
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