Cellular and molecular abnormalities have been identified in Mecp2 mutant mice that likely contribute to the ASD-like phenotypes. Both Mecp2tm1.1Bird and Mecp2tm1.1Jae mice have cortical neurons with decreased spine density (Belichenko et al., 2009), and Mecp2tm1.1Bird mice have decreased dendritic complexity (Fukuda et al., 2005). Similar results have been reported in Mecp2tm1.1Jae hippocampus (Smrt et al., 2007), but this varies across development: spine density is decreased at postnatal day seven but returns to wild type levels by postnatal day 15 (Chapleau et al., 2012). Moreover, adult Mecp2tm1Hzo mice have normal spine density and dendritic complexity in both cortex and hippocampus (Moretti et al., 2006). More recently, it was demonstrated that neurons in somatosensory cortex of Mecp2tm1.1Jae mice are more stable than controls at postnatal day 25–26 (P25–P26), as assessed by in vivo two-photon imaging (Landi et al., 2011).
