The study presents a method for generating three-dimensional human forebrain spheroids that mimic the dorsal and ventral forebrain, containing glutamatergic and GABAergic neurons. These spheroids can be assembled to model the saltatory migration of interneurons similar to that observed in fetal forebrain. The research demonstrates that in Timothy syndrome, a neurodevelopmental disorder caused by mutations in the CaV1.2 calcium channel, interneurons display abnormal migratory saltations. The study also shows that after migration, interneurons functionally integrate with glutamatergic neurons to form a microphysiological system. This approach provides a valuable tool for studying development and disease, and for deriving spheroids that resemble other brain regions to assemble circuits in vitro. The study also demonstrates the integration of interneurons into a synaptically-connected microphysiological system without the need for seeding onto rodent cortical cultures or brain slices. The findings suggest that the migration defect in interneurons carrying the TS gain-of-function mutation can be restored by reducing the activity of LTCCs. The study also highlights the potential of this approach for studying the interaction of specific neuronal cell types and for generating and probing neural circuits within personalized human microphysiological systems.The study presents a method for generating three-dimensional human forebrain spheroids that mimic the dorsal and ventral forebrain, containing glutamatergic and GABAergic neurons. These spheroids can be assembled to model the saltatory migration of interneurons similar to that observed in fetal forebrain. The research demonstrates that in Timothy syndrome, a neurodevelopmental disorder caused by mutations in the CaV1.2 calcium channel, interneurons display abnormal migratory saltations. The study also shows that after migration, interneurons functionally integrate with glutamatergic neurons to form a microphysiological system. This approach provides a valuable tool for studying development and disease, and for deriving spheroids that resemble other brain regions to assemble circuits in vitro. The study also demonstrates the integration of interneurons into a synaptically-connected microphysiological system without the need for seeding onto rodent cortical cultures or brain slices. The findings suggest that the migration defect in interneurons carrying the TS gain-of-function mutation can be restored by reducing the activity of LTCCs. The study also highlights the potential of this approach for studying the interaction of specific neuronal cell types and for generating and probing neural circuits within personalized human microphysiological systems.