Moreover, the available evidence strongly supports dysfunctional synapses as a component of autism pathophysiology. However, although there are widespread disruptions in synaptic function across the mouse models of ASD, the direction of change and magnitude of effect are inconsistent between different models, as well as between different types of synapses within any given model. Although there are many apparent differences between models, it is difficult to compare results that were reported in different brain regions or at different times during development. For instance, Fmr1 knockout mice have decreased spine stability somatosensory cortex (Cruz-Martin et al., 2010), whereas Mecp2tm1.1Jae mice have increased spine stability in the same region (Landi et al., 2011), but the former study used mice that were postnatal day 10–12, whereas the latter study used mice that were postnatal day 25–26. Therefore, more side-by-side comparisons of different mouse models of ASDs would be valuable. One interesting discovery from genetics studies of ASDs is the frequent mutations in genes encoding epigenetic machinery. However, it is not immediately clear how deficiency of these proteins contributes to autism pathophysiology. As has
