Mutations in the GRIN2D gene, encoding one of the subunits of NMDA receptor (NMDAR), are associated with developmental and epileptic encephalopathies (DEE). The clinical presentation of DEE includes epilepsy, motor and cognitive deficits, developmental delay, and a high mortality rate. Grin2d mice carrying the pathogenic V667I variant recapitulate key phenotypes of the human disease.To explore the effect of the Grin2d mutation on neuronal and synaptic functions, we used acute cerebellum brain slices recorded from wild-type (WT) and Grin2d mice. We recorded neuronal activity from Purkinje neurons, inhibitory neurons critical for motor and cognitive functions.Extracellular recordings demonstrated a decrease in the frequency of spontaneous firing of action potentials in Grin2d mice on postnatal day (P) 8-14. Whole-cell current clamp recordings at this age also showed aberrant firing with early after-depolarization (EAD)-like events in Grin2d mice. Nevertheless, the frequency of spontaneous firing was corrected over development and was similar between WT and Grin2d mice after P21. Analysis of spontaneous inhibitory postsynaptic potentials (iPSPs) onto Purkinje cells demonstrated similar basal sIPSPs. Bath application of NMDA enhanced the frequency of iPSPs, with an augmented response in Grin2d mice, which was more pronounced in the P21 and P35 Grin2d mice. Together, these data demonstrate neuronal, synaptic, and developmental changes in the cerebellum of Grin2d mutant mice that are not limited to NMDAR. Uncovering the differences in circuit activity will further our understanding of GRIN2D-DEE disease mechanisms and may highlight potential new treatment avenues.