NAc receive dopamine (DA) projections from the ventral tegmental area (VTA) (Björklund and Dunnett, 2007, Ikemoto, 2007, Morales and Margolis, 2017) and this pathway play a major role in motivated behaviours, reinforcement learning and reward processing (Hamid et al., 2016; Salamone and Correa, 2012; Schultz, 2016; Watabe-Uchida et al., 2017). Like any other process, there are negative feedback pathways to balance the projections and prevent overexpression of DA. This arise from various structures (Matsui et al., 2014) but recent studies show that NAc is the main source of this inhibitory input (GABAergic input) (Beier et al., 2015; Watabe-Uchida et al., 2012). There were few conflicting results on this with studies suggesting inputs from NAc to VTA to be disinhibiting (Bocklisch et al., 2013; Chuhma et al., 2011; Xia et al., 2011) and a recent study addressing that NAc synapse onto VTA GABA as well as DA neurons via GABA-A receptor (GABAAR) and GABA-B receptor (GABABR) respectively (Edward et al., 2017). This, however, also projects a different result compared to the study done by Paladini in 1999 where inhibitory responses from the striatum to DA neurons were blocked by GABA-A antagonist hinting at pathway mediated by GABA-A instead.

In this particular study by Hongbin et al. in 2017, the shell component of the NAc is further subdivided into medial shell (NAcMed) and lateral shell (NAcLat). D1-MSN in the NAcMed is found inhibiting NAcMed-projecting DA neurons via GABAAR while NAcLat-projecting DA neurons via GABABR. D1-MSNs in the NAcLat, on the other hand, projects onto VTA GABA to result in disinhibition of NAcL