outside of their home cage). Furthermore, a previous study using in situ hybridization in mice also showed induction of c-Fos in D1+ and D2+ MSNs in dStr, although in this study representative bar graphs show greater number of D1+ c-Fos positive neurons (Ferguson et al., 2006). Interestingly, this study reveals significantly enhanced c-Fos induction in D2+ MSNs in the dStr after loss of ERK1, which parallels our findings of enhanced c-Fos induction in D2+ MSNs specifically in the NAc shell after disruption of BDNF signaling which is known to enhance ERK activity (Lobo et al., 2010). However, opposite behavioral responses to cocaine were observed in each study, which may reflect induction of c-Fos in D2+ MSNs in dStr vs. NAc shell. Finally, previous literature using in situ hybridization/immunohistochemistry in rats has shown acute psychostimulants can induce c-Fos equally in both MSNs when the drug is given in a novel environment (Badiani et al., 1999; Uslaner et al., 2001a,b; Ferguson and Robinson, 2004) and chronic administration of amphetamine is reported to selectively induce c-Fos in D2+ MSNs (Mattson et al., 2007). These different results could be a reflection of the experimental procedures used (in situ hybridization vs. GFP reporter mice) or
