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Abstract
We have produced a mouse strain in which the deletion of the NMDAR1 gene is restricted
to the CA1 pyramidal cells of the hippocampus by using a new and general method that
allows CA1-restricted gene knockout. The mutant mice grow into adulthood without obvious
abnormalities. Adult mice lack NMDA receptor-mediated synaptic currents and long-term
potentiation in the CA1 synapses and exhibit impaired spatial memory but unimpaired
nonspatial learning. Our results strongly suggest that activity-dependent modifications
of CA1 synapses, mediated by NMDA receptors, play an essential role in the acquisition
of spatial memories.