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Article Dans Une Revue Journal of Neuroscience Année : 2012

Interaction between αCaMKII and GluN2B controls ERK-dependent plasticity.

Farida El Gaamouch
  • Fonction : Auteur
Alain Buisson
  • Fonction : Auteur
Olivier Moustie
  • Fonction : Auteur
Mado Lemieux
  • Fonction : Auteur
Simon Labrecque
  • Fonction : Auteur
Paul de Koninck
  • Fonction : Auteur

Résumé

Understanding how brief synaptic events can lead to sustained changes in synaptic structure and strength is a necessary step in solving the rules governing learning and memory. Activation of ERK1/2 (extracellular signal regulated protein kinase 1/2) plays a key role in the control of functional and structural synaptic plasticity. One of the triggering events that activates ERK1/2 cascade is an NMDA receptor (NMDAR)-dependent rise in free intracellular Ca(2+) concentration. However the mechanism by which a short-lasting rise in Ca(2+) concentration is transduced into long-lasting ERK1/2-dependent plasticity remains unknown. Here we demonstrate that although synaptic activation in mouse cultured cortical neurons induces intracellular Ca(2+) elevation via both GluN2A and GluN2B-containing NMDARs, only GluN2B-containing NMDAR activation leads to a long-lasting ERK1/2 phosphorylation. We show that αCaMKII, but not βCaMKII, is critically involved in this GluN2B-dependent activation of ERK1/2 signaling, through a direct interaction between GluN2B and αCaMKII. We then show that interfering with GluN2B/αCaMKII interaction prevents synaptic activity from inducing ERK-dependent increases in synaptic AMPA receptors and spine volume. Thus, in a developing circuit model, the brief activity of synaptic GluN2B-containing receptors and the interaction between GluN2B and αCaMKII have a role in long-term plasticity via the control of ERK1/2 signaling. Our findings suggest that the roles that these major molecular elements have in learning and memory may operate through a common pathway.

Dates et versions

hal-01159970 , version 1 (04-06-2015)

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Citer

Farida El Gaamouch, Alain Buisson, Olivier Moustie, Mado Lemieux, Simon Labrecque, et al.. Interaction between αCaMKII and GluN2B controls ERK-dependent plasticity.. Journal of Neuroscience, 2012, 32 (31), pp.10767-79. ⟨10.1523/JNEUROSCI.5622-11.2012⟩. ⟨hal-01159970⟩

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