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- Title
Interaction Between &agr;CaMKII and GluN2B Controls ERK-Dependent Plasticity.
- Authors
Gaamouch, Farida El; Buisson, Alain; Moustié, Olivier; Lemieux, Mado; Labrecque, Simon; Bontempi, Bruno; De Koninck, Paul; Nicole, Olivier
- Abstract
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 ERKl/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 ERKl/2 cascade is an NMDA receptor (NMDAR)-dependent rise in free intracellular Ca2+ concentration. However the mechanism by which a short-lasting rise in Ca2+ concentration is transduced into long-lasting ERKl/2-dependent plasticity remains unknown. Here we demonstrate that although synaptic activation in mouse cultured cortical neurons induces intracellular Ca2+ elevation via both GluN2A and GluN2B-containing NMDARs, only GluN2B-containing NMDAR activation leads to a long-lasting ERKl/2 phosphorylation. We show that aCaMKII, but not ßCaMKII, is critically involved in this GluN2B-dependent activation of ERKl/2 signaling, through a direct interaction between GluN2B and aCaMKII. We then show that interfering with GluN2B/aCaMKII 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 aCaMKII have a role in long-term plasticity via the control of ERKl/2 signaling. Our findings suggest that the roles that these major molecular elements have in learning and memory may operate through a common pathway.
- Subjects
PROTEIN kinases; NEUROPLASTICITY; LABORATORY mice; NEURON analysis; CELLULAR signal transduction; PHOSPHORYLATION; CALMODULIN
- Publication
Journal of Neuroscience, 2012, Vol 32, Issue 31, p10767
- ISSN
0270-6474
- Publication type
Article
- DOI
10.1523/JNEUROSCI.5622-11.2012