Deficits in reward processing are a characteristic symptomatic dimension of psychiatric diseases such as major depression, bipolar disorder and schizophrenia. These deficits have been linked to the dysfunction of the mesocorticolimbic dopamine transmission suggesting the existence of common underlying pathophysiological mechanisms. Numerous clinical studies have described a decrease in n-3 polyunsaturated fatty acids (PUFAs) in subpopulations of patients suffering from psychiatric disorders (Conklin et al., 2010; Messamore and McNamara, 2016). Moreover, preclinical results from our laboratory and others suggest that dopamine (DA) transmission is particularly sensitive to PUFA biostatus (Chalon et al. 2006, Ducrocq et al. 2020). However, a causal link between PUFA biostatus, the integrity of DA transmission, and specific symptomatic dimensions remain to be established. We have demonstrated that a developmental deficiency in n-3 PUFAs in mice does lead to reward processing deficits with motivational impairments in a progressive ratio task as well as increased impulsivity in a delayed discounting task. Additionally, we have identified a disruption in the mesocorticolimbic DA dynamics under n-3 PUFA deficiency, measured via DA sensor d-light coupled with fiber photometry. These changes seem to be associated with a reorganization of DA projections within this circuit that were revealed trough quantitative immunofluorescence analysis of DA fibers in mesocorticolimbic structures i.e. in the prefrontal cortex and the nucleus accumbens. Finally, we show that normalizing the levels of PUFAs specifically in DA neurons is sufficient to restore behavioral performance, confirming a causal link between n-3 PUFAs deficiency, integrity of DA transmission, and reward processing deficits.