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Modulation of AMPA receptor surface diffusion restores hippocampal plasticity and memory in Huntington’s disease models
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Modulation of AMPA receptor surface diffusion restores hippocampal plasticity and memory in Huntington’s disease models
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Journal Article
Modulation of AMPA receptor surface diffusion restores hippocampal plasticity and memory in Huntington’s disease models
2018
Overview
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.
Cognitive decline in Huntington’s disease (HD) may be due to impaired hippocampal synaptic plasticity. In this study the authors show that AMPA receptor surface diffusion, a key player in synaptic plasticity, is deregulated in multiple HD mouse models as a result of impaired BDNF signalling that underlies the memory deficits, and can be pharmacologically rescued.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/51
/ 13/95
/ 14/63
/ 9/30
/ Animals
/ Brain
/ Brain-derived neurotrophic factor
/ Brain-Derived Neurotrophic Factor - metabolism
/ Defects
/ Hippocampus - physiopathology
/ Humanities and Social Sciences
/ Huntington Disease - metabolism
/ Huntington Disease - pathology
/ Huntington Disease - physiopathology
/ Kinases
/ Long-Term Potentiation - drug effects
/ Memory
/ Neuronal Plasticity - drug effects
/ Neuronal Plasticity - physiology
/ Postsynaptic density proteins
/ Protein Transport - drug effects
/ Proteins
/ Receptors, AMPA - metabolism
/ Science
/ Signal Transduction - drug effects
/ Tyrosine
/ α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid
/ α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors
