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© Research
Publication : Nature communication

Modulation of AMPA receptor surface diffusion restores hippocampal plasticity and memory in Huntington’s disease models

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Nature communication - 15 Oct 2018

Zhang HY, Zhang CL, Vincent J, Zala D, Benstaali C, Sainlos M, Grillo-Bosch D, Daburon S, Coussen F, Cho Y, David DJ, Saudou F, Humeau Y & Choquet D

Link to Pubmed [PMID] – PMC6189172

Nature Communications: Volume 9, Article number: 4272 (2018)

Impaired hippocampal synaptic plasticity contributes to cognitive impairment in Huntington’s disease (HD). However, the molecular basis of such synaptic plasticity defects is not fully understood. Combining live-cell nanoparticle tracking and super-resolution imaging, we show that AMPAR surface diffusion, a key player in synaptic plasticity, is disturbed in various rodent models of HD. We demonstrate that defects in the brain-derived neurotrophic factor (BDNF)–tyrosine receptor kinase B (TrkB) signaling pathway contribute to the deregulated AMPAR trafficking by reducing the interaction between transmembrane AMPA receptor regulatory proteins (TARPs) and the PDZ-domain scaffold protein PSD95. The disturbed AMPAR surface diffusion is rescued by the antidepressant drug tianeptine via the BDNF signaling pathway. Tianeptine also restores the impaired LTP and hippocampus-dependent memory in different HD mouse models. These findings unravel a mechanism underlying hippocampal synaptic and memory dysfunction in HD, and highlight AMPAR surface diffusion as a promising therapeutic target.

https://www.nature.com/articles/s41467-018-06675-3