The function of neural circuits depends on the precise connectivity between populations of neurons. In the central nervous system (CNS) this is mediated by glutamatergic and GABAergic synapses, and there is emerging evidence that disruptions in the formation or function of excitatory or inhibitory synapses lead to excitation/inhibition (E/I) imbalances, which characterize several psychiatric and neurodevelopmental disorders [1–8]. These considerations underscore the importance of understanding the molecular control of excitatory and inhibitory synapse formation, and the signals that allow cell type-specific control of E/I balance.
