Besides the anatomic observation of deficient astrocytic maturation in SCZ hGPC chimeras, our genomic analysis of SCZ-derived hGPCs revealed the significant down-regulation in hGPCs derived from all 4 SCZ patients of a number of synaptic genes, including neuroligin-3, neuroexophilin-1, and LINGO1 relative to their normal controls (Table S3; Figure 5). Other synapse-associated genes, such as neurexin-1 and DSCAML1 were significantly and sharply down-regulated in GPCs derived from 3 patients (lines 8, 29, and 51) but not in the fourth (line 164). Similarly, SLITRKs 2–5 were significantly and sharply down-regulated in GPCs derived from 3 patients (lines 8, 51, and 164), but not in a fourth (line 29), which was instead associated with sharp down-regulation of LINGO1, DSCAML1, and several neurexins and neuroexophilins; these data suggesting the heterogeneity of transcriptional dysfunction that may lead to a final common pathway of glial-involved 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
