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The expression of NMDA receptor subunit NR3A is high in the neonatal brain but low in adults. However, its functional role in the adult brain is obscure. Using wild-type (WT) and NR3A knockout (KO) mice, we show here that NR3A plays imperative roles in multiple behavioral functions in adults. NR3A deletion produced a slow locomotor phenotype with enhanced memory capacities. Hippocampal slices from juvenile and adult NR3A KO mice showed greater long-term potentiation (LTP) compared to WT slices. NR3A deletion resulted in increased expression and phosphorylation of calmodulin-dependent kinase II (CaMKII). CaMKII inhibition abrogated the enhanced LTP in NR3A KO slices. NR3A KO mice were also more sensitive to acute and chronic pain. These data reveal for the first time that NR3A, despite its low expression, plays several critical roles in behavioral activities in adults and may be a therapeutic target for modulating behaviors under normal and pathological conditions.

Slow in Motion but Smart in Learning and Memory: Behavioral Changes in Adult NR3A Knockout Mice