of social interactivity or primary perception – human glial chimeras acquire new causal associations more quickly than do allografted or untransplanted controls (Han et al., 2013). Thus, engrafted human GPCs and their daughter glia can integrate into, and substantially modify, developing neural networks (Franklin and Bussey, 2013). On that basis, we postulated that the disruption in normal glial development noted in our SCZ glial chimeras might yield disease-associated changes in learning and behavior. To address this question, we assessed the behavioral phenotypes of immunodeficient but otherwise wild-type mice neonatally engrafted with SCZ GPCs, relative to matched hosts engrafted with control-derived GPCs. For these experiments, we used normally-myelinated hosts rather than shiverer mice, so as to produce mice chimeric only for human GPCs and astrocytes, and not for oligodendroglia, thus isolating any observed behavioral effects to SCZ hGPCs and astrocytes.
