Executive function impairments are a common symptom of many psychiatric pathologies. They are correlated with impaired dopaminergic transmission originating from the midbrain within the medial prefrontal cortex (mPFC), and subcortical areas such as the nucleus accumbens (NAc). This mesocorticolimbic dopamine transmission is believed to be a key modulator of goal-directed behaviors and reward processing through its action on dopaminoceptive neurons expressing either D1 (D1R) or D2 receptors (D2R) in those target structures. However, the precise mechanisms by which this transmission enables an individual to flexibly adapt its behavior remain unclear. Through a chemogenetic approach, we show that this dopaminergic pathway is crucial for the animal's ability to adapt to changes in the contingencies between actions and outcomes. From a mechanistic standpoint, we demonstrate using interfering peptides that mPFC and NAc D1/NMDA and D2/NMDA receptor heteromers constitute a central mechanism to mediate such effects of dopamine on executive functions. Using a calcium sensor approach coupled with fiber photometry, we characterized the neural signature of mPFC dopaminoceptive neurons expressing D1R or D2R during Pavlovian and operant conditioning paradigms and the effect of heteromer blockade on these activities. We identified specific patterns of activity during discrete cue, action and consumption phases, and found that blockade of either D1/NMDA or D2/NMDA heteromers strongly impacts activity patterns during reversal of contingencies. These data provide a better understanding of the underlying mechanisms of behavioral adaptations and suggest that D1/NMDA and D2/NMDA heteromers could be prime targets for the development of more specific therapeutic treatments.