The essential role of hippocampal CA1 NMDA receptor-dependent synaptic plasticity in spatial memory.
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.
Tsien
J Z
JZ
Howard Hughes Medical Institute, Center for Learning and Memory, Massachusetts Institute of Technology, Cambridge 02139, USA.
Huerta
P T
PT
Tonegawa
S
S
D000818:Animals; D001522:Behavior, Animal / Q000502:physiology; D018891:Dentate Gyrus / Q000502:physiology; D005818:Genetic Engineering / Q000379:methods; D005822:Genetic Vectors; D006624:Hippocampus / Q000502:physiology*; D017403:In Situ Hybridization; D017774:Long-Term Potentiation; D008568:Memory / Q000502:physiology*; D051379:Mice; D018345:Mice, Knockout; D009473:Neuronal Plasticity / Q000502:physiology*; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology*; D009435:Synaptic Transmission
D016194:Receptors, N-Methyl-D-Aspartate