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Researchers at University of Lyon Have Reported New Data on Intercellular Junctions

May 20, 2014

By a News Reporter-Staff News Editor at Life Science Weekly -- Fresh data on Intercellular Junctions are presented in a new report. According to news originating from Lyon, France, by NewsRx correspondents, research stated, "Abstract NMDA-type glutamate receptors (NMDAR) are central actors in the plasticity of excitatory synapses. During adaptive processes, the number and composition of synaptic NMDAR can be rapidly modified, as in neonatal hippocampal synapses where a switch from predominant GluN2B- to GluN2A-containing receptors is observed after the induction of long-term potentiation (LTP)."

Our news journalists obtained a quote from the research from the University of Lyon, "However, the cellular pathways by which surface NMDAR subtypes are dynamically regulated during activity-dependent synaptic adaptations remain poorly understood. Using a combination of high-resolution single nanoparticle imaging and electrophysiology, we show here that GluN2B-NMDAR are dynamically redistributed away from glutamate synapses through increased lateral diffusion during LTP in immature neurons. Strikingly, preventing this activity-dependent GluN2B-NMDAR surface redistribution through cross-linking, either with commercial or with autoimmune anti-NMDA antibodies from patient with neuropsychiatric symptoms, affects the dynamics and spine accumulation of CaMKII and impairs LTP. Interestingly, the same impairments are observed when expressing a mutant of GluN2B-NMDAR unable to bind CaMKII. We thus uncover a non-canonical mechanism by which GluN2B-NMDAR surface dynamics plays a critical role in the plasticity of maturing synapses through a direct interplay with CaMKII. Synopsis image Long-term potentiation in immature hippocampal neurons requires glutamate receptor lateral diffusion and CaMKII recruitment, a process that can be blocked by autoimmune anti-NMDAR antibodies from patients with neuropsychiatric symptoms. In the hippocampus, postsynaptic NMDA receptor surface dynamics is locally regulated during plasticity. GluN2B-NMDA receptor surface dynamics is required for synaptic long-term potentiation. Surface GluN2B-NMDA receptor and CAMKII constantly influence each other."

According to the news editors, the research concluded: "Decreased surface NMDA receptor dynamics, and thus impaired synaptic long-term potentiation, is likely the basis of cognitive symptoms in anti-NMDA receptor autoimmune disorder."

For more information on this research see: Surface dynamics of GluN2B-NMDA receptors controls plasticity of maturing glutamate synapses. Embo Journal, 2014;33(8):842-861. Embo Journal can be contacted at: Wiley-Blackwell, 111 River St, Hoboken 07030-5774, NJ, USA (see also Intercellular Junctions).

The news correspondents report that additional information may be obtained from J.P. Dupuis, University of Lyon, F-69365 Lyon, France. Additional authors for this research include L. Ladepeche, H. Seth, L. Bard, J. Varela, L. Mikasova, D. Bouchet, V. Rogemond, J. Honnorat, E. Hanse and L. Groc.

Keywords for this news article include: Lyon, Antibodies, France, Europe, Synapses, Glutamates, Immunology, Cell Membrane, Glutamic Acid, Blood Proteins, Immunoglobulins, Cellular Structures, Intercellular Junctions

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Source: Life Science Weekly

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