N-methyl-D-aspartate (NMDA) receptors are ionotropic glutamate receptors that play important roles in synaptic transmission in the central nervous system. They are essential for learning and memory formation, and they are key regulators of neuroplasticity. De novo mutations in the genes that encode these receptors can cause GRIN-related disorders, which result in neurological symptoms including epilepsy, intellectual disabilities, and movement disorders. My thesis studies involve characterizing disease-related variants at the Tyr647 residue of the GluN1 subunit, which is obligatory in NMDA receptor assembly. This residue is part of the strictly conserved activation gate. I hypothesize that the disease-related variants alter NMDA receptor function by disrupting the gating mechanism, and thus disrupting synaptic transmission, which can result in the pathological phenotypes seen in patients who carry these variants. I use electrophysiological techniques to learn more about NMDA receptors, including cell-attached voltage patch clamp and murine brain slice electrophysiology.