The brain utilizes neurons and glia to construct neural circuitry, generated and fine-tuned by the formation of numerous plastic synapses. Subtle aberrant changes during development in the spatiotemporal-patterning or synaptic function of specific neuronal subtypes can perturb this complex neuronal connectivity [1], and thus likely contribute to neuropsychiatric diseases such as schizophrenia (SZ) [2,3]. Both human postmortem studies and mouse models of SZ have demonstrated reduced dendritic arborization and synaptic density associated with SZ [4–6]. However, mouse models fail to recapitulate the polygenic effect of disease, and postmortem studies are frequently confounded by factors such as patient medication history, drug/alcohol abuse or environmental stressors and are further limited to the study of the endpoint of disease [7]. Now, human induced pluripotent stem cell (hiPSC)-based models present the ability to generate nearly limitless numbers of patient-derived neurons for the study of disease initiation and progression.
