In contrast to glutamate, there is a lack of research on GABA function in the two MSNs in addiction models, which is surprising considering both ethanol and benzodiazepines enhance the effects of GABA and the two MSNs receive dense GABAergic inputs as stated above. There is also considerable evidence pointing to enhanced inhibition in the NAc at least after chronic cocaine exposure (White et al., 1995; Peoples et al., 1998; Zhang et al., 1998; Thomas et al., 2001; Beurrier and Malenka, 2002). Heiman et al. (2008) performed high throughput genetic screening in the two MSNs after chronic cocaine exposure and, interestingly, the most altered biological process in the D1+ MSNs was GABA signaling. In particular, there was potent upregulation of GABAA receptor subunits Gabra1 and Gabra4 as well as the GABAB receptor subunit Gabrb3, and this group found that chronic cocaine increases the frequency of small-amplitude GABAergic mini inhibitory postsynaptic currents (mIPSCs) in D1+ MSNs (Heiman et al., 2008). On the other hand, another group recently showed that chronic cocaine results in an opposite response with decreased frequency and amplitude
