Alcohol use disorder (AUD) is characterized by compulsive binge alcohol intake, leading to
various health and social harms. Protein Kinase C epsilon (PKCε), a specific family of PKC isoenzyme,
regulates binge alcohol intake, and potentiates alcohol-related cues. Alcohol via upstream kinases
like the mammalian target to rapamycin complex 1 (mTORC1) or 2 (mTORC2), may affect the activities
of PKCε or vice versa in AUD. mTORC2 phosphorylates PKCε at hydrophobic and turn motif,
and was recently reported to be associated with alcohol-seeking behavior, suggesting the potential role
of mTORC2-PKCε interactions in the pathophysiology of AUD. mTORC1 regulates translation of
synaptic proteins involved in alcohol-induced plasticity. Hence, in this article, we aimed to review the
molecular composition of mTORC1 and mTORC2, drugs targeting PKCε, mTORC1, and mTORC2 in
AUD, upstream regulation of mTORC1 and mTORC2 in AUD and downstream cellular mechanisms
of mTORCs in the pathogenesis of AUD.
Faculty Opinions recommendation of Metabolic turnover of synaptic proteins: kinetics, interdependencies and implications for synaptic maintenance.
