Abstract
Long term potentiation (LTP) at hippocampal Schaffer collateral-CA1 synapses involves an early and a late phase, where only the latter is sensitive to protein synthesis inhibitors. Here we characterized the dynamics of protein synthesis associated with the induction of L-LTP using a transgenic mouse model in which a cAMP responsive element (CRE)-regulated promoter drives production of an enhanced yellow fluorescent protein (eYFP). We found that eYFP fluorescence increased after less than 30 min following L-LTP induction. Application of transcription and translation suppressors and the NMDA receptor antagonist D-AP5 inhibited the L-LTP and prevented the rise in eYFP levels. The early-phase of LTP was not affected by inhibiting protein synthesis.
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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2-Amino-5-phosphonovalerate / pharmacology
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Animals
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Bacterial Proteins / metabolism
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Electric Stimulation / methods
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Electrophysiology / methods
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Excitatory Amino Acid Antagonists / pharmacology
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Gene Expression Regulation / drug effects
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Gene Expression Regulation / physiology*
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Hippocampus / cytology*
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Hippocampus / drug effects
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In Vitro Techniques
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Long-Term Potentiation / drug effects
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Long-Term Potentiation / physiology*
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Luminescent Proteins / metabolism
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Mice
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Mice, Transgenic
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Potassium Channels, Voltage-Gated / metabolism
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Promoter Regions, Genetic / physiology
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Protein Synthesis Inhibitors / pharmacology
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Pyramidal Cells / drug effects
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Pyramidal Cells / metabolism*
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Shaw Potassium Channels
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Time Factors
Substances
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Bacterial Proteins
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Excitatory Amino Acid Antagonists
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Kcnc1 protein, mouse
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Luminescent Proteins
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Potassium Channels, Voltage-Gated
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Protein Synthesis Inhibitors
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Shaw Potassium Channels
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yellow fluorescent protein, Bacteria
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2-Amino-5-phosphonovalerate