Ppp1r2-cre/fGluN1 knockout mice or simply KO mice was generated as previously described (15). Briefly, the protein phosphatase 1, regulatory subunit 2 (Ppp1r2)-cre line was bred to a loxP-flanked GluN1 line (16) to elicit the GluN1 deletion from the postnatal second week in a subset of cortical and hippocampal Ppp1r2-positive interneurons, a majority of which are parvalbumin-containing. Double in situ hybridization immunocytochemistry showed that, at postnatal day 14, no GluN1 mRNA was detected in ~30% of Cre-targeted interneurons in the S1 cortex of Ppp1r2-Cre/homozygously-floxed-GluN1 knockout mice (Zhang S., BS, unpublished, 2012). GluN1 deletion appeared to be completed by postnatal day 21. In contrast, there was no GluN1 deletion in the homozygously-floxed GluN1 (fGluN1 or flox) or Ppp1r2-cre littermate control mice. All mice were maintained after backcrossing to C57BL/6NTac (B6) strain six times. Female KO mice were crossed with homozygously-floxed GluN1 male mice. Wild-type B6 mice were also used for PGC-1α in situ hybridization.
