Recently, we reported that mice lacking GIRK2 in forebrain pyramidal neurons (CaMKIICre(+):Girk2 fl/fl mice) were deficient in contextual fear learning, a hippocampal-dependent behavior6. As CaMKIICre(+):Girk2 fl/fl mice exhibited a loss of GIRK-dependent signaling in dorsal but not ventral CA1 pyramidal neurons6, we asked whether viral restoration of GIRK2a or GIRK2c in dorsal CA1 pyramidal neurons of CaMKIICre(+):Girk2 fl/fl mice could rescue normal fear learning. Adult CaMKIICre(+):Girk2 fl/fl mice received bilateral infusions of Cre-dependent variants of the GIRK2a and GIRK2c expression viruses into the dorsal CA1 (Fig. 7A). After a suitable post-surgical recovery period (2 wk), we tested the efficacy of our viral treatment by measuring baclofen-induced somato-dendritic currents in CA1 pyramidal neurons in acutely isolated slices. Currents in dorsal CA1 pyramidal neurons from CaMKIICre(+):Girk2 fl/fl mice treated with control virus were small (Fig. 7B,C), and comparable in size to those reported previously for untreated CaMKIICre(+):Girk2 fl/fl mice6. Dorsal CA1 pyramidal neurons from CaMKIICre(+):Girk2 fl/fl mice expressing GIRK2a or GIRK2c exhibited significantly larger baclofen-induced currents (Fig. 7B,C). Indeed, currents measured in dorsal CA1 pyramidal neurons expressing GIRK2a or GIRK2c were notably
