Schematic depicting a simple working hypothesis of how the nucleus accumbens (NAc) may regulate rewarding and aversive states. (a) NAc neurons tonically inhibit reward-related processes. Under normal circumstances, there is a balance between cortical (PFC, AMG) excitatory (+) influences mediated by glutamate actions at AMPA and NMDA receptors, and midbrain (VTA) inhibitory (−) influences mediated by dopamine actions at D2-like receptors. NAc neurons have low baseline rates of firing, and depolarization-mediated influx of Ca2+ through NMDA receptors and calcium channels is not sufficient to alter gene expression. (b) Depolarization of NAc neurons containing D2-like receptors and enkephalin inhibits downstream areas implicated in reward (e.g., vental pallidum) which is encoded as aversion. It also leads to elevated Ca2+ influx, which may trigger experience-dependent neuroadaptations (e.g., activation of CREB, elevated expression of GluR1) can produce feed-forward effects that dysregulate the system. AMG, amygdala; Ca, calcium channel; Ca2+, calcium; CREB, cAMP response element binding protein; D2, dopamine D2-like receptor; DA, dopamine; ENK, enkephalin; G1/G2, AMPA glutamate receptor containing GluR1 and GluR2; GABA, gamma-aminobutyric acid; GLU, glutamate; N, NMDA receptor; NAc, nucleus accumbens; PFC, prefrontal cortex; VTA, ventral tegmental area