not require elements within the Girk2 promoter or untranslated domains in the Girk2 mRNAs, as only coding sequence was included in the viral reconstitution vectors. The unique GIRK2c C-terminus is also not required, as both GIRK2a and GIRK2c were similarly impacted by morphine treatment. Interestingly, the strengthening of GIRK-dependent signaling in VTA dopamine neurons evoked by burst firing was blocked by inclusion of a peptide mimic of the GIRK2c (and GIRK3) C-terminal domain60. These data indicate that the GIRK2c C-terminal domain may be a critical determinant of plasticity involving specific GIRK channel subtypes, including the GIRK1-lacking channels expressed in midbrain dopamine neurons13, 31.
