induced in D2+ MSNs in the NAc shell after withdrawal in response to the context-specific association with morphine (Borgkvist et al., 2008). The precise functional role of pERK in drug addiction remains to be determined. Pharmacological treatment with ERK inhibitors has been shown to decrease cocaine reward, however, a knockout of ERK1 potentiates cocaine reward, suggesting that ERK inhibitors may preferentially be affecting ERK2. Recently, we showed that optogenetic activation of D1+ MSNs in the NAc, which increases an animal’s rewarding responses to cocaine, potently reduces both pERK1 and pERK2. Future studies manipulating ERK expression in a cell-type-specific manner are necessary to fully address the functional role of ERK signaling in the two MSNs in drug abuse.
