We next asked whether the SCZ hGPCs that prematurely entered the gray matter differentiated instead into astrocytes in that environment, or whether they rather manifested an impairment in lineage progression that prevented their astrocytic differentiation as well. Both SCZ and control hGPC-engrafted shiverer brains were immunostained for astrocytic glial fibrillary acidic protein (GFAP) at 19 weeks after neonatal graft, using a species-specific anti-human GFAP antibody. We found that astrocytic maturation from engrafted hGPCs was markedly deficient in the SCZ hGPC-engrafted brains (n=19, derived from 3 SCZ patient lines, and n=12 control mice, from 3 control patients) (Figures 3A–B). In the callosal white matter, as well as in both the striatal and cortical gray matter, astrocytic differentiation by SCZ hGPCs was significantly less than that of control GPCs, such that whereas all control hGPC forebrains showed dense human GFAP+ astrocytic maturation, far fewer SCZ hGPCs manifested hGFAP expression and astrocytic phenotype (controls: 6,616 ± 672.3 GFAP+ cells/mm3 in callosum, n=12; SCZ: 1,177 ± 276.6 GFAP+ callosal cells/mm3, n=19; p<0.0001 by 2-way t-test (Figure 3C). This defect in astrocytic differentiation was consistently
