Abstract
The hippocampal CA1 region is crucial for converting new memories into long-term memories, a process believed to continue for week(s) after initial learning. By developing an inducible, reversible, and CA1-specific knockout technique, we could switch N-methyl-D-aspartate (NMDA) receptor function off or on in CA1 during the consolidation period. Our data indicate that memory consolidation depends on the reactivation of the NMDA receptor, possibly to reinforce site-specific synaptic modifications to consolidate memory traces. Such a synaptic reinforcement process may also serve as a cellular means by which the new memory is transferred from the hippocampus to the cortex for permanent storage.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Comment
MeSH terms
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Animals
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Conditioning, Psychological
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Doxycycline / pharmacology
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Excitatory Postsynaptic Potentials
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Fear
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Green Fluorescent Proteins
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Hippocampus / physiology*
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Long-Term Potentiation
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Luminescent Proteins / biosynthesis
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Maze Learning
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Memory / physiology*
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Mice
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Mice, Knockout
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Mice, Transgenic
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Receptors, AMPA / physiology
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Receptors, N-Methyl-D-Aspartate / genetics
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Receptors, N-Methyl-D-Aspartate / physiology*
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Retention, Psychology
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Synapses / physiology*
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Synaptic Transmission
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Time Factors
Substances
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Luminescent Proteins
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NR1 NMDA receptor
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Receptors, AMPA
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Receptors, N-Methyl-D-Aspartate
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Green Fluorescent Proteins
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Doxycycline