indirect pathways; Gerfen, 1984, 1992). Early work suggested that drugs of abuse exert most influence on the D1+ MSNs, with the use of numerous dopamine receptor agonists and antagonists providing important insight into the functional and molecular roles of each MSN in drug reward behaviors (Self, 2010). However, current cell-type-specific methodologies, including fluorescent reporter mice that express GFP under D1 or D2 bacterial artificial chromosomes (BACs; Gong et al., 2003; Valjent et al., 2009; gensat.org), conditional mouse models such as the use of tetracycline-regulated inducible transgenic mice (Chen et al., 1998; Kelz et al., 1999), and transgenic mice expressing Cre-recombinase using D1 or D2 BACs, yeast artificial chromosomes (YACs), or knock-in mice (Gong et al., 2007; Lemberger et al., 2007; Heusner et al., 2008; Parkitna et al., 2009; Valjent et al., 2009; Bateup et al., 2010; Lobo et al., 2010; gensat.org) as well as cell-type-specific viral-mediated gene transfer (Cardin et al., 2010; Hikida et al., 2010; Lobo et al., 2010; Ferguson et al., 2011), have provided profound new insight into the precise molecular underpinnings of each MSN subtype and their regulation by drugs of abuse (Table 1).
