A number of research groups have manipulated the expression of MeCP2 in mouse brains temporally and spatially using various Cre lines to determine potential brain regions, cell types, and developmental time periods involved in Rett syndrome pathogenesis. Conditional knockout (KO) of Mecp2 using either the brain-specific Nestin-Cre line in which the recombinase is activated during embryonic development or the forebrain-specific CamK-Cre93 line in which the recombinase is activated postnatally recapitulate the phenotypes observed in the conventional Mecp2 mutant mice (Chen et al., 2001). A subsequent study found that Mecp2 deficiency in excitatory neurons of the forebrain using CamKII-Cre93 mice also produce ASD-like features (Gemelli et al., 2006). However, other studies provide evidence that loss of MeCP2 specifically in GABAergic neurons (Viaat-Cre) is sufficient (Chao et al., 2010). Thus, loss of MeCP2 in a subset of either excitatory or inhibitory neurons can lead to ASD-like features. It remains unclear whether the deficiency of MeCP2 in these excitatory or inhibitory neurons disrupts the same circuits. Using mice engineered with a stop codon surrounded by loxP sites crossed with a ubiquitously-expressed inducible Cre
