be a result of high energetic demand on MSNs to maintain a hyperpolarized state, a possible mechanism of vulnerability of striatal MSNs proposed in Huntington’s disease115. We also found OUD-associated changes in neuronal energetics with the downregulation of nicotinamide riboside kinase 1, NMRK1, and the basic helix-loop-helix family member e40, BHLHE40 (DEC1), both of which are involved in regulating cellular metabolism, oxidative stress, and inflammation81. Together, the broad set of changes in genes and pathways associated with OUD were associated with various processes involved in cell stress.
