Background/Aims: Acute sodium depletion by the combination of pharmacological natriuresis via furosemide administration and a sodium-deficient diet results in a strong induction of salt appetite in rats. Recent evidence suggests that acute furosemide decreases both dopamine uptake and striatal dopamine transporter density and increases enkephalin mRNA levels in the nucleus accumbens (Acb). Therefore, it has been hypothesized that the motivational/attentional circuit in the brain is activated in salt-appetitive rats. Methods: To determine which loci along the dopaminergic circuit are responsible for this behavior, 10–15 min before furosemide-treated adult male Sprague-Dawley rats were allowed 2-hour access to 2% salt solution (2-bottle choice), we pharmacologically blocked dopamine receptor subtype 1 (D1r) and subtype 2 (D2r) with SCH23390 or raclopride, respectively, and stimulated D1r with SKF81297 or D2r with quinpirole in the shell of the Acb (AcbSh). Furthermore, delta opioid receptors were blocked with naltrindole in the AcbSh or ventral tegmental area (VTA). Results: We found that microinjections (1 µg) of SCH23390, raclopride, SKF81297, quinpirole, or naltrindole into the AcbSh had no effect. However, infusion of naltrindole into the VTA attenuated salt intake, whereas [D-Ser<sup>2</sup>,Leu<sup>5</sup>,Thr<sup>6</sup>]-enkephalin had no effect. Additionally, in rats previously primed with furosemide to crave salt in a ‘need-free’ manner, salt intake was augmented in the VTA and reduced in the AcbSh after infusion of [D-Ser<sup>2</sup>,Leu<sup>5</sup>,Thr<sup>6</sup>]-enkephalin. Conclusion: These data provide evidence that mesolimbic opioid systems are involved in the facilitation of salt-appetitive behavior.