The role of the lateral orbitofrontal cortex (LOFC) in ethanol drinking is examined.
Excitotoxic lesions of the LOFC did not affect drinking in non-dependent mice.
In alcohol-dependent mice, lesioned mice drank more ethanol.
A similar effect was observed in mice expressing an inhibitory DREADD receptor in the LOFC.
LOFC dysfunction may be one factor driving excessive alcohol consumption.