Current understanding of the rewarding and addictive effects of opioids involves mu-opioid receptor (MOR) binding within the nucleus accumbens (NAcc), a region of the basal forebrain. GABA neurons in the NAcc are thought to function to potentiate the rewarding response to opioids, and in fact, drugs that generally stimulate GABAergic activity are also addictive, a phenomenon mediated in part by endogenous opioid systems. It is still unclear how some individuals become susceptible to opioid addiction and thus, further understanding of the interaction between the MOR and other neurotransmitter systems in the reward pathway is needed. We report here evidence supporting the direct interaction between GABA and MOR within the mouse NAcc. Male and female FVB/NJ mice (12-16 months of age) were euthanized via carbon dioxide inhalation and brains processed for histology and immunohistochemistry (IHC). Coronal sections (10-12 um in thickness) were taken through the NAcc at the level of the anterior commissure. A mouse monoclonal antibody against GAD67, an enzyme catalyzing GABA production, was used in conjunction with an anti-mouse rhodamine red-X-labeled secondary antibody to identify GABA neurons. Alternating sections were stained for MOR using a rabbit polyclonal MOR1 antibody linked to the fluorophore FITC. The location of expression of GAD67 and MOR1 was identified using a DAPI nuclear stain. As expected, fluorescence microscopy results show that GAD67 staining is localized predominately in the cytoplasm. Unexpectedly, the MOR1-FITC stain tended to localize in the cytoplasm and cell membrane, but more prominently within the nucleus and nuclear membrane. In separate experiments, we used double-immunostaining to study the co-expression of MOR1 and GAD67 within the same NAcc neurons. A similar localization pattern for these proteins was detected. There are few published reports of GAD67 and MOR1 co-expression within neurons of the NAcc. Previous studies of MOR expression show the receptor to be localized to the plasma membrane and, to a smaller degree, intracellularly. Here we found the MOR1 staining to be predominantly in the nucleus and nuclear membrane. Further studies are required to validate the nuclear expression of MOR in GABAergic NAcc neurons. We conclude that individual mouse NAcc neurons may express both MOR1 and GAD67, potentially providing a functional link between opioid and GABAergic systems in the reward pathway.