CCAAT Enhancer Binding Protein   Plays an Essential Role in Memory Consolidation and Reconsolidation

A. A. Arguello, X. Ye, O. Bozdagi, G. Pollonini, S. Tronel, D. Bambah-Mukku, G. W. Huntley, D. Platano, C. M. Alberini
Journal of Neuroscience. 2013-02-20; 33(8): 3646-3658
DOI: 10.1523/jneurosci.1635-12.2013

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A newly formed memory is temporarily fragile and becomes stable through a process
known as consolidation. Stable memories may again become fragile if retrieved or
reactivated, and undergo a process of reconsolidation to persist and strengthen.
Both consolidation and reconsolidation require an initial phase of transcription
and translation that lasts for several hours. The identification of the critical
players of this gene expression is key for understanding long-term memory
formation and persistence. In rats, the consolidation of inhibitory avoidance
(IA) memory requires gene expression in both the hippocampus and amygdala, two
brain regions that process contextual/spatial and emotional information,
respectively; IA reconsolidation requires de novo gene expression in the
amygdala. Here we report that, after IA learning, the levels of the transcription
factor CCAAT enhancer binding protein δ (C/EBPδ) are significantly increased in
both the hippocampus and amygdala. These increases are essential for long-term
memory consolidation, as their blockade via antisense
oligodeoxynucleotide-mediated knockdown leads to memory impairment. Furthermore,
C/EBPδ is upregulated and required in the amygdala for IA memory reconsolidation.
C/EBPδ is found in nuclear, somatic, and dendritic compartments, and a dendritic
localization of C/EBPδ mRNA in hippocampal neuronal cultures suggests that this
transcription factor may be translated at synapses. Finally, the induction of
long-term potentiation at CA3-CA1 synapses by tetanic stimuli in acute slices, a
cellular model of long-term memory, leads to an accumulation of C/EBPδ in the
nucleus. We conclude that the transcription factor C/EBPδ plays a critical role
in memory consolidation and reconsolidation.

Auteurs Bordeaux Neurocampus