Schizophrenia (SZ) is a severe and persistent psychiatric disorder influenced by genetic factors. A recent exome-sequencing study of schizophrenia identified 10 genes as having an exome-wide significant excess of rare damaging coding variants. Of these variants, protein truncating variants (PTVs) of the XPO7 gene conferred the highest SZ risk. XPO7 encodes exportin 7, a protein that gates nucleocytoplasmic transport. XPO7 is expressed in neurons, but its role in the brain is completely unknown. To assess the role of XPO7 in neuronal development and function, XPO7 knock-down (KD) was induced in pyramidal neurons of layers II/III of the frontal cortex by in utero electroporation of shRNA at embryonic stage E14.5. We first observed that, although most XPO7 KD neurons migrated correctly, some displayed abnormal localization in lower cortical layers. The proliferation of neural progenitors was increased upon XPO7 KD, potentially contributing to localization defects. Furthermore, using patch-clamp to study the physiological properties of neurons that had correctly reached layer II/III of the cortex, we observed that XPO7 KD led to neuronal hyper-excitability. XPO7 KD neurons also displayed a reduction in the frequency of miniature synaptic excitatory and inhibitory currents, indicating decreased synaptic input. Finally, we also noted a slower deactivation of NMDA receptors-mediated currents, reflecting a gain of function. These findings underscore the crucial role of XPO7 in regulating neuronal proliferation, neuronal excitability, and synaptic function, and may provide insight into SZ pathogenesis.