Modeling the Neurocircuitry Involved in Binge Drinking

Binge drinking is marked by an initial intense and rapid consumption of alcohol, followed by a prolonged period of lower-rate maintenance drinking. However, the neural circuitry that drives and regulates these phases is not fully understood. Researchers have now created a computational model that connects key brain regions involved in binge drinking.

The model includes cortical Seek (mPFC) and Go (insula) populations that form a loop of mutual excitation. A SetPoint population integrates information from striatal activity, serving as an internal estimate of effort and consumption. The model also comprises ventral (nucleus accumbens, NAc) and dorsal (dorsolateral striatum, DLS) striatal populations, as well as a VTA population that provides transient reward-prediction signals via dopamine.

Using firing-rate formalism with noisy dynamics, the researchers were able to replicate the two-phase binge pattern. They found that the PFC-insula loop functions as a bistable module, initiating and maintaining the initial high-intensity phase of drinking. Meanwhile, feedback from the striatum to the SetPoint population governs the timing of the shift from front-loading to sustained drinking, without affecting the intensity of the binge.

The researchers also discovered that the magnitude of the VTA dopamine transient directly influences the intensity of the initial binge phase. Through sensitivity analyses, they identified PFC-insula connectivity, VTA-to-NAc modulation, and striato-cortical feedback as crucial parameters that determine whether the two-phase binge pattern persists or is disrupted.

These findings offer a mechanistic framework for understanding binge-like alcohol intake in terms of specific circuit motifs. The researchers propose that these neural circuits could be targeted in interventions for alcohol use disorder.