synaptic dysfunction in SCZ (Tables S2 and S3). These transcripts are critical contributors to synaptic stabilization and function (Sudhof, 2008), but while typically considered neuronal, may be produced significantly by glial cells as well (Zhang et al., 2014). The relative down-regulation of these genes by SCZ hGPCs may reflect the suppression of mature glial transcripts in these cells, coincident with their relative block in glial differentiation. This in turn may lead to a relative failure of SCZ hGPCs and their derived astrocytes to provide these key proteins to their neuronal partners, as well as a potential failure on the part of glial progenitors receiving synaptic inputs to respond to afferent stimulation (De Biase et al., 2010; Lin and Bergles, 2004). Thus, besides the structural havoc that might be expected of a cortical connectome formed without normal astrocytic support, the synaptic structure of the resultant networks might be expected to be destabilized by poor SCZ glial provision to the synaptic cleft of key astrocytic proteins required for normal synaptic maintenance and function.
