al., 2013). This type of finding may lead to understanding epigenetic changes associated with schizophrenia as well as potential therapeutic targets. Oscillatory activity in the EEG of mice selectively bred to respond positively to alcohol administration resembles event-related time-frequency findings in humans in some respects (although not others), lending credence to mouse models of alcoholism (Criado & Ehlers, 2009) and suggesting routes to understanding time-frequency endophenotypes in humans. In addition, delayed latency of the N1 EEG or MEG response is a putative endophenotype for autism spectrum disorders (ASD). A recent investigation found that the N1 response in the right hemisphere was delayed in children with ASD relative to typically developing children, as expected. Investigators also observed a latency delay of virtually the same magnitude in mice treated prenatally with valproic acid (VPA), an insult-based mouse model of autism. This latency delay was inversely correlated with inter-trial phase locking of gamma activity in both species. Moreover, expression levels of messenger RNA for the autism risk gene neuroligin-3 (NLGN3), which are reduced in mice exposed to VPA, were associated with gamma phase locking in mice as well. Thus, this study suggests the possibility that an autism endophenotype may be related to an
