Abstract
Gene-targeted mice lacking the AMPA receptor subunit GluR-A (also called GluR1 encoded by the gene Gria1,) have deficits in hippocampal CA3-CA1 long-term potentiation (LTP) and have profoundly impaired hippocampus-dependent spatial working memory (SWM) tasks, although their spatial reference memory remains normal. Here we show that forebrain-localized expression of GFP-tagged GluR-A subunits in GluR-A-deficient mice rescues SWM, paralleling its rescue of CA3-CA1 LTP. This provides powerful new evidence linking hippocampal GluR-A-dependent synaptic plasticity to rapid, flexible memory processing.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Analysis of Variance
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Animals
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Behavior, Animal / physiology
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Cell Count / methods
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Disease Models, Animal
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Green Fluorescent Proteins / metabolism
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Hippocampus / cytology
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Hippocampus / physiopathology
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Immunohistochemistry / methods
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In Vitro Techniques
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Indoles
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Long-Term Potentiation / genetics
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Memory Disorders / genetics*
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Memory Disorders / physiopathology
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Memory Disorders / therapy
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Memory, Short-Term / physiology*
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Mice
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Mice, Knockout
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Pyramidal Cells / physiology
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Receptors, AMPA / deficiency*
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Receptors, AMPA / genetics
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Space Perception / physiology*
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Transduction, Genetic*
Substances
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Indoles
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Receptors, AMPA
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Green Fluorescent Proteins
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DAPI
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glutamate receptor ionotropic, AMPA 1