Many of the studies investigating putative roles that PAC plays in addictive disorders have centered on drug effects on the medial prefrontal cortex (mPFC), a core part of the brain reward system that has been shown to be intimately involved with alcohol and drug-related learning and memory (Abernathy et al., 2010; Sun et al., 2011). Increased theta-gamma PAC strength within prelimbic cortex, a part of mPFC, has been demonstrated in heroin addicted rats during conditioned place preference (Zhu et al., 2019). Rats trained to associate cocaine delivery with foot shock persisted in cocaine seeking behavior after inactivation of prelimbic cortex by GABA agonists highlighting the role this part of the mPFC plays in terminating motivated behaviors that are harmful or noxious (Limpens et al., 2015). Moreover, long-term alcohol use appears to modify the mPFC in such a way to facilitate impulsive or compulsive behaviors, co-morbid features of AUD (Klenowski, 2018). The mPFC appears to encode the intention to drink alcohol, and when contribution of mPFC in decision-making to drink alcohol is diminished, subcortical brain regions involved in habitual behaviors are possibly left as primary driver of alcohol consumption (Linsenbardt et al., 2019).