Neuronal firing is modulated by different types of local oscillatory activity. Theta oscillation is one of those found in the mammalian hippocampus during exploratory behavior and REM sleep. Theta oscillation is thought to separate functional states of the network along time and provide time windows for neurons to be involved in different memory processes. It is well-known that principal cells in the hippocampus fire preferentially at a specific phase of theta oscillation, which is a phenomenon termed as theta phase locking. While previous studies suggest that inhibitory input plays a role in theta phase locking, it has not been well investigated how excitatory input contributes to it. In this study, we focused on NMDA receptor, which is a type of ionotropic glutamate receptor and is involved in multiple types of synaptic plasticity, and examined its role in theta phase locking and other firing properties of CA1 principal cells. For this purpose, we devised recombinant adeno-ascociated viral vectors to achieve local RNA interference against NR1 gene, which encodes an essential subunit to form functional NMDA receptor. We achieved virus transduction in a minor portion of CA1 area of rats and performed tetrode-based unit and local field potential recording from the virus-transduced area. This approach allowed us to monitor the activity of NR1-ablated neurons in freely behaving rats. The NR1-ablated neurons showed higher variability in locking phase during theta oscillation indicating that NMDA receptor regulates temporal allocation of neuronal firing along theta oscillation. Thus, NMDA-receptor-dependent synaptic plasticity may contribute to theta phase locking by making neurons more susceptible for firing at a preferred phase. In addition, we found impairment in spatially-modulated firing (place-cell activity), which suggest that temporal and spatial properties of neuronal firing in the CA1 may be mechanistically linked by NMDA receptor.