Dysfunction of the mPFC has been repeatedly found in populations of subjects that drink alcohol excessively (Schacht et al., 2013). Exposure to experience- or experimentally paired alcohol cues, increases neuronal activity within the PFC (George et al., 2001; Tapert et al., 2003; Kareken et al., 2010), and the magnitude of this effect is correlated with increases in self-reported alcohol craving (Myrick et al., 2004) and relapse (Grüsser et al., 2004). Additionally, recently abstinent individuals with an AUD exhibit reduced baseline neuronal activity within the mPFC (Catafau et al., 1999). Similar effects are observed in rodents, with exposure to alcohol-associated cues eliciting reinstatement of extinguished alcohol seeking and robust increases in biomarkers of neural activity in PFC (Dayas et al., 2007; Groblewski et al., 2012; Pfarr et al., 2015). More recent reports suggest a critical role for the PFC in alcohol extinction learning (Cannady et al., 2017; Keistler et al., 2017), suggesting that this brain region may be critically involved in “remapping” associations between alcohol-associated stimuli and the motivational properties of alcohol. Thus, preclinical rodent and human data converge to implicate altered function of PFC in AUD.
