In adults NMDAR are critical for excitatory neurotransmission and learning and plasticity in cortical circuits. These receptors are also targets of attack in some patients with autoimmune encephalitis. In these patients, there is prominent, progressive circuit dysfunction. In this talk, I will describe our efforts to understand the roles of NMDAR in developmental cortical circuit formation using the somatosensory callosal projection as a model. Strikingly, we have found that NMDAR, when removed genetically or by antibody infusion, are required for proper formation of the callosal projection. The phenotype appears to be a loss of axonal repulsion and we have determined that NMDAR collaborate with EphrinB/EphB signaling to allow proper formation of this circuit.