Collectively, the data provided herein indicate differences in the role of the mPFC in alcohol consumption between populations with or without increased familial risk of excessive drinking. This finding is characterized by two primary features observed in P rats. (1) The encoding of the decision to drink is blunted during alcohol drinking. (2) And the encoding of stimuli previously associated with alcohol is enhanced during water sessions. We have also observed that neurons in the mPFC of P rats may be uniquely sensitive to the alcohol-associated context of the 2CAP conditioning chamber (i.e., before task; Linsenbardt and Lapish, 2015). The expression of these features was observed in animals that exhibit an inherited risk for excessive drinking, which may reflect underlying differences in neurobiology that facilitate persistent alcohol seeking and/or the transition to aversion-resistant drinking. Identifying strategies to restore the contribution of the mPFC in the intention to drink alcohol and blunt the encoding of alcohol associated cues observed in water sessions may provide effective targets to treat an AUD. Importantly these data further highlight the need to consider inherited/genetic risk factors when developing treatment strategies for AUDs.
