The Persistence of Hippocampal-Based Memory Requires Protein Synthesis Mediated by the Prion-like Protein CPEB3
Langue
EN
Article de revue
Ce document a été publié dans
Neuron. 2015-06-17, vol. 86, n° 6, p. 1433-1448
Résumé en anglais
Consolidation of long-term memories depends on de novo protein synthesis. Several translational regulators have been identified, and their contribution to the formation of memory has been assessed in the mouse hippocampus. ...Lire la suite >
Consolidation of long-term memories depends on de novo protein synthesis. Several translational regulators have been identified, and their contribution to the formation of memory has been assessed in the mouse hippocampus. None of them, however, has been implicated in the persistence of memory. Although persistence is a key feature of long-term memory, how this occurs, despite the rapid turnover of its molecular substrates, is poorly understood. Here we find that both memory storage and its underlying synaptic plasticity are mediated by the increase in level and in the aggregation of the prion-like translational regulator CPEB3 (cytoplasmic polyadenylation element-binding protein). Genetic ablation of CPEB3 impairs the maintenance of both hippocampal long-term potentiation and hippocampus-dependent spatial memory. We propose a model whereby persistence of long-term memory results from the assembly of CPEB3 into aggregates. These aggregates serve as functional prions and regulate local protein synthesis necessary for the maintenance of long-term memory.< Réduire
Mots clés en anglais
Animals
Anxiety
Exploratory Behavior
Fear
Glutamic Acid
Hippocampus
In Vitro Techniques
Locomotion
Long-Term Potentiation
Male
Maze Learning
Memory
Mice
Mutation
Neurons
Phosphopyruvate Hydratase
Reaction Time
RNA-Binding Proteins
Mice Inbred C57BL
Mice Transgenic
Conditioning Psychological
Unités de recherche