, 2004). The assumption is that these underlying pathophysiological mechanisms also disrupt cortical function during wakefulness,
alter perception and behavior, and may generate autistic behavioral symptoms. While our study cannot pinpoint the underlying pathophysiological mechanism(s), the results do suggest that such mechanisms may exist in putative language areas at very early stages of autism development. Our results are compatible with several recent reports of reduced resting-state synchronization in adolescents and adults with autism (Anderson et al., 2011, Cherkassky et al., 2006, Kennedy and Courchesne, 2008, Monk et al., 2009 and Weng et al., 2010). Most importantly, one recent BKM120 cost study has reported that adults and adolescents with autism exhibit significantly decreased interhemispheric synchronization in multiple cortical areas, including a
similar IFG area to the one described here (see Figure 3 in Anderson et al., 2011). One speculative possibility is that reduced interhemispheric synchronization found during early autism development may persist and become even more widespread with age. Further studies GS-1101 solubility dmso exploring other aspects of cortical and subcortical synchronization are warranted for determining the spatial specificity of synchronization abnormalities 3-mercaptopyruvate sulfurtransferase throughout autism development. Converging evidence from multiple fields of neurobiology, not just neuroimaging, suggests that autism is a disorder of abnormal neural connectivity and synchronization (Levy et al., 2009). Genetic studies have reported abnormalities in genes associated with synaptic formation, maturation, and transmission in autism, which are expected to generate abnormally connected neural networks in individuals with autism (Geschwind and Levitt, 2007 and Rubenstein and Merzenich, 2003). Electrophysiology studies
in mouse models of autism have reported neural network abnormalities, including excitation-inhibition imbalances (Gibson et al., 2008) and abnormal synaptic transmission (Etherton et al., 2009). Anatomical MRI studies have reported increased white matter volumes (Herbert et al., 2004) along with abnormal white matter myelination (Alexander et al., 2007 and Ben Bashat et al., 2007). Finally, several fMRI studies in adults and adolescents with autism have reported abnormal synchronization across brain areas under active task conditions (Hasson et al., 2009 and Jones et al., 2010) or spontaneously fluctuating during rest/sleep (Anderson et al., 2011, Cherkassky et al., 2006, Kennedy and Courchesne, 2008, Monk et al., 2009 and Weng et al., 2010).