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The Journal of Neuroscience, October 19, 2005, 25(42):9581-9590; doi:10.1523/JNEUROSCI.2423-05.2005

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Cellular/Molecular
The Translation Repressor 4E-BP2 Is Critical for eIF4F Complex Formation, Synaptic Plasticity, and Memory in the Hippocampus

Jessica L. Banko,^1 * Francis Poulin,^3 * Lingfei Hou,¹ Christine T. DeMaria,³ Nahum Sonenberg,^3 * and Eric Klann^1,2 *

Departments of ¹Molecular Physiology and Biophysics and ²Neuroscience, Baylor College of Medicine, Houston, Texas 77030, and ³Department of Biochemistry, McGill University, Montreal, Quebec, Canada H3G 1Y6

Long-lasting synaptic plasticity and memory requires mRNA translation, yet little is known as to how this process is regulated. To explore the role that the translation repressor 4E-BP2 plays in hippocampal long-term potentiation (LTP) and learning and memory, we examined 4E-BP2 knock-out mice. Interestingly, genetic elimination of 4E-BP2 converted early-phase LTP to late-phase LTP (L-LTP) in the Schaffer collateral pathway, likely as a result of increased eIF4F complex formation and translation initiation. A critical limit for activity-induced translation was revealed in the 4E-BP2 knock-out mice because L-LTP elicited by traditional stimulation paradigms was obstructed. Moreover, the 4E-BP2 knock-out mice also exhibited impaired spatial learning and memory and conditioned fear-associative memory deficits. These results suggest a crucial role for proper regulation of the eIF4F complex by 4E-BP2 during LTP and learning and memory in the mouse hippocampus.

Key words: LTP; protein synthesis; hippocampus; Morris water maze; learning and memory; fear conditioning

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Received June 14, 2005; revised August 25, 2005; accepted August 30, 2005.

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