Newswise — Decades of clinical and pre-clinical studies have demonstrated that chronic drinking leads to long-lasting changes in reward- and stress-related neuronal circuitry. The nucleus accumbens (NAc) is an important part of this circuitry. Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) are commonly used by neuroscientists to identify signals in nerve circuits that specify certain behaviors, perceptions, emotions, innate drives, or motor functions. This rodent study investigated the effects of DREADDs on nerve cell activity in the NAc (comprised of a core and a shell) in relation to binge-like drinking.

Researchers injected the brains of female C57BL/6J mice – a strain that is genetically predisposed to a high preference for alcohol – with three AAV vectors (viruses that carry genes to targeted areas). Two weeks later, the brains of one group of mice were measured for specific chemical-induced (called CNO) changes in NAc activity. Other groups of mice had their binge-like drinking or taste-enhanced fluid intake assessed using a limited-access Drinking in the Dark (DID) schedule.

CNO increased firing in certain NAc cells (called hM3Dq) and decreased firing in other NAc cells (called hM4Di), confirming the role that these cells play in altering neuronal activity both spatially and temporally. Increasing activity in the entire NAc, or just the core of the NAc, was sufficient to decrease binge drinking.  The effect was not evident when only the NAc shell was manipulated.  Further, the reduction in drinking was not due to general malaise, an altered perception of taste, or reduced calorie seeking.  The authors of the study noted that this first round of evidence supporting the bidirectional control of the NAc and its effects on drinking has promising implications for the treatment of binge drinking and its consequences.