to cocaine (Brown et al., 2010). An additional induction requirement for this drug-evoked synaptic plasticity is activation of NMDARs on the DA neurons. This conclusion is based on the observations that systemic administration of an NMDAR antagonist blocks the plasticity (Ungless et al., 2001) as does ablation of the critical NMDAR subunit NR1 selectively in DA neurons (Engblom et al., 2008; Zweifel et al., 2008). A simple model that can explain all of these results is that DA receptor activation on VTA DA neurons leads to an increase in NMDAR EPSCs and that this in turn facilitates the generation of NMDAR-dependent LTP (Schilstrom et al., 2006).
