Significance: HeterozygousNRXN1deletions predispose to schizophrenia and other neurodevelopmental disorders. Engineered heterozygousNRXN1deletions impair neurotransmitter release in human neurons, suggesting a synaptic pathophysiological mechanism. In a multicenter effort to test the generality and robustness of this pivotal observation, we used, at two laboratories, independent analyses of patient-derived and newly engineered human neurons with heterozygousNRXN1deletions. Schizophrenia patient-derived neurons withNRXN1deletions exhibited the same major decrease in neurotransmitter release and an increase in CASK protein as engineered human neurons withNRXN1deletions. Strikingly, engineered mouseNrxn1-deficient neurons derived by the same method displayed no such phenotype, suggesting a human-specific role forNRXN1. Thus, heterozygousNRXN1deletions robustly impair synaptic function in human neurons, enabling future drug discovery efforts.

A small amount of HClO₄spraying treatment can pull the flexible anode's Fermi level down, substantially decrease the sheet resistance, and induce an intimate contact at interfaces, suitable for fabricating high-performance flexible organic solar cells.