ethanol exposure. Excessive ethanol consumption potentiates glutamatergic transmission via a postsynaptic mechanism at the corticostriatal input and involves a presynaptic mechanism at the amygdalostriatal input (Ma et al., 2017). Chronic ethanol consumption strengthens glutamatergic input to D1-, but not D2-, receptor-expressing DMS MSNs, and GABAergic synaptic strength is enhanced specifically onto D2 MSNs (Cheng et al., 2017; Wang et al., 2015). Interestingly, a bottom-up-approach study following from these findings demonstrated that chemo-genetic excitation of DMS D1 MSNs or inhibition of D2 MSNs promotes ethanol consumption in mice (Cheng et al., 2017).
