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The Translation Repressor 4E-BP2 Is Critical for eIF4F Complex Formation, Synaptic Plasticity, and Memory in the Hippocampus
Abstract
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.
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“Third, changes in the induction of the late phase of LTP as well as learning deficits have also been reported in mice lacking 4E-BP2, which also show increased mTOR-dependent translational initiation[27](#R27).”
From Reversal of learning deficits in a Tsc2+/− mouse model of tuberous sclerosis (2008) · cites this paper as [27]
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BackgroundSynaptic tagging: implications for late maintenance of hippocampal long-term potentiation
Frey, U., & Morris, R. G. M. (1998) · Trends in Neurosciences · doi:10.1016/s0166-2236(97)01189-2 · Cited by 615
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Sorted by citations
Regulation of Translation Initiation in Eukaryotes: Mechanisms and Biological Targets
Sonenberg, N., & Hinnebusch, A. G. (2009) · Cell · doi:10.1016/j.cell.2009.01.042 · Cited by 3,304
“These results were interpreted to mean that the excessive translation could be deleterious to the synaptic plasticity required for learning and memory (Banko et al., 2005).”
Self-citationmTOR signaling: At the crossroads of plasticity, memory and disease
Hoeffer, C. A., & Klann, E. (2010) · Trends in Neurosciences · doi:10.1016/j.tins.2009.11.003 · Cited by 1,128
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Costa-Mattioli, M., Sossin, W. S., Klann, E., & Sonenberg, N. (2009) · Neuron · doi:10.1016/j.neuron.2008.10.055 · Cited by 944
Self-citationReversal of learning deficits in a Tsc2+/− mouse model of tuberous sclerosis
Ehninger, D., Han, S., Shilyansky, C., Zhou, Y., Li, W., Kwiatkowski, D. J., Ramesh, V., & Silva, A. J. (2008) · Nature Medicine · doi:10.1038/nm1788 · Cited by 882
The mTOR pathway in the control of protein synthesis
Wang, X., & Proud, C. G. (2006) · Physiology · doi:10.1152/physiol.00024.2006 · Cited by 778
Metadata
- Authors
- Banko, J. L., Poulin, F., Hou, L., DeMaria, C. T., Sonenberg, N., & Klann, E.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2005-10-19
- Volume
- 25
- Issue
- 42
- Pages
- 9581-9590
- ISSN
- 0270-6474
- 1529-2401
- Cited by
- 290
- References
- 4
- Language
- en
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