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The nucleus accumbens (<jats:styled-content style=\"fixed-case\">NA<\/jats:styled-content>c) is an integral component of this circuitry. Here, we investigate the effects of<jats:styled-content style=\"fixed-case\">DREADD<\/jats:styled-content>s (Designer Receptors Exclusively Activated by Designer Drugs) on neuronal activity in the<jats:styled-content style=\"fixed-case\">NA<\/jats:styled-content>c and binge\u2010like drinking.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>C57<jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content>\/6J mice were stereotaxically injected with<jats:styled-content style=\"fixed-case\">AAV<\/jats:styled-content>2<jats:styled-content style=\"fixed-case\">hS<\/jats:styled-content>yn\u2010<jats:styled-content style=\"fixed-case\">HA hM<\/jats:styled-content>3Dq, \u2010<jats:styled-content style=\"fixed-case\">hM<\/jats:styled-content>4Di, or \u2010<jats:styled-content style=\"fixed-case\">eGFP<\/jats:styled-content>bilaterally into<jats:styled-content style=\"fixed-case\">NA<\/jats:styled-content>c [core\u00a0+\u00a0shell, core or shell]. We measured clozapine\u2010<jats:italic>n<\/jats:italic>\u2010oxide (CNO)\u2010induced changes in<jats:styled-content style=\"fixed-case\">NA<\/jats:styled-content>c activity and assessed binge\u2010like ethanol (EtOH) or tastant\/fluid intake in a limited access Drinking in the Dark (<jats:styled-content style=\"fixed-case\">DID<\/jats:styled-content>) schedule.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>We found that<jats:styled-content style=\"fixed-case\">CNO<\/jats:styled-content>increased<jats:styled-content style=\"fixed-case\">NA<\/jats:styled-content>c firing in<jats:styled-content style=\"fixed-case\">hM<\/jats:styled-content>3Dq positive cells and decreased firing in<jats:styled-content style=\"fixed-case\">hM<\/jats:styled-content>4Di cells, confirming the efficacy of these channels to alter neuronal activity both spatially and temporally. Increasing<jats:styled-content style=\"fixed-case\">NA<\/jats:styled-content>c core\u00a0+\u00a0shell activity decreased binge\u2010like drinking without altering intake of other tastants. Increasing activity specifically in the<jats:styled-content style=\"fixed-case\">NA<\/jats:styled-content>c core reduced binge\u2010like drinking, and decreasing activity in the<jats:styled-content style=\"fixed-case\">NA<\/jats:styled-content>c core increased drinking. Manipulation of<jats:styled-content style=\"fixed-case\">NA<\/jats:styled-content>c shell activity did not alter<jats:styled-content style=\"fixed-case\">DID<\/jats:styled-content>. Thus, we find that increasing activity in the entire<jats:styled-content style=\"fixed-case\">NA<\/jats:styled-content>c, or just the<jats:styled-content style=\"fixed-case\">NA<\/jats:styled-content>c core is sufficient to decrease binge drinking.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>We conclude that the reduction in EtOH drinking is not due to general malaise, altered perception of taste, or reduced calorie\u2010seeking. Furthermore, we provide the first evidence for bidirectional control of<jats:styled-content style=\"fixed-case\">NA<\/jats:styled-content>c core and binge\u2010like drinking. 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