The ambition of this proposal is to identify the cellular underpinnings of the early transition between casual to sustain drinking using drinking-in-the-dark model. We propose to employ a variety of complementary approaches, including mouse genetics, optogenetics, behavior and biophysical approaches to test the overarching hypothesis that computing of the synaptic strength of cortical and amygdala inputs (a phenomenon also known as synaptic gating) is a mechanism enabling nucleus accumbens medium spiny neurons to integrate cognitive and emotional information, and is modulated by alcohol exposure to control consumption. We postulate that this cellular mechanism contributes to the vulnerability of adolescents to binge drinking.