Journal
JOURNAL OF NEUROSCIENCE
Volume 30, Issue 17, Pages 5830-5842Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.0119-10.2010
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Funding
- Telethon, Italy [GGP06208]
- Fondazione Cariplo [2006-0779]
- Compagnia di San Paolo [2005, 1964]
- European Community [LSHM-CT-2004-511995]
- PRIN (Progetto di Ricerca di Interesse Nazionale)
- CNR RTSL (Consiglio Nazionale delle Ricerche Ricerca Scientifica a Tema Libero)
- Giovanni Armenise-Harvard Foundation
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Activity-dependent changes in synaptic structure and spine morphology are required for learning and memory, and depend on protein translation. We show that the kinase for eukaryotic elongation factor 2 (eEF2K) regulates dendritic spine stability and synaptic structure by modulating activity-dependent dendritic BDNF synthesis. Specifically RNAi knockdown of eEF2K reduces dendritic spine stability and inhibits dendritic BDNF protein expression; whereas overexpression of a constitutively activated eEF2K induces spine maturation and increases expression of dendritic BDNF. Furthermore, BDNF overexpression rescues the spine stability reduced by RNAi knockdown of eEF2K. We also show that synaptic activity-dependent spine maturation and dendritic BDNF protein expression depend on mGluR/EF2K-induced eEF2 phosphorylation. We propose that the eEF2K/eEF2 pathway is a key biochemical sensor that couple neuronal activity to spine plasticity, by controlling the dendritic translation of BDNF.
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