Dopamine signals modulate NAc activity via complex interactions between D1- and D2-like dopamine receptors (Hu & White, 1997; Ikemoto et al., 1997). For example, NAc neurons periodically exhibit ‘up states’ during which action potentials may occur (O’Donnell, 2003) which dopamine can facilitate while simultaneously reducing firing rate (Goto & O’Donnell, 2001). Additionally, dopamine is a modulator of striatal GABAergic interneuron coupling, indirectly affecting cell firing patterns (Cummings et al., 2008). This action increases the signal-to-baseline of phasically active neurons resulting in stronger efferent signals. Indeed, inactivation of VTA neurons decreases NAc phasic excitations for reward predictive cues (Yun et al., 2004). Thus, it may be the case the neurons that exhibit pre versus post response activity relative the reinforced response may represent different sets of NAc neurons defined by differential distribution of D1 versus D2 receptors and projection targets (Gertler et al., 2008). As such, the ability of dopamine to drive NAc neurons that encode distinct aspects of cocaine-reinforced responding (PR, RFe, RFi) may be related to dopamine receptor distribution on those cells, but likely also is a function of the ability of dopamine to modulate distinct afferent inputs that in turn drive select populations of NAc neurons.
