AMPAR Removal Underlies Aβ-Induced Synaptic Depression and Dendritic Spine Loss
| Autor: | Roberto Malinow, Taisuke Tomita, Takeshi Iwatsubo, Jannic Boehm, Helen Hsieh, Chihiro Sato, Sangram S. Sisodia |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
Patch-Clamp Techniques
Dendritic Spines Neuroscience(all) Immunoblotting HUMDISEASE Enzyme-Linked Immunosorbent Assay AMPA receptor Biology Receptors Metabotropic Glutamate Transfection p38 Mitogen-Activated Protein Kinases MOLNEURO Article Synaptic augmentation mental disorders Image Processing Computer-Assisted Animals Receptors AMPA Phosphorylation Long-term depression Cells Cultured Neurons SYSBIO Amyloid beta-Peptides Neuronal Plasticity Synaptic scaling Alphavirus Infections General Neuroscience Excitatory Postsynaptic Potentials Long-term potentiation DNA Endocytosis Rats Electrophysiology Synaptic fatigue nervous system Mutation Synapses Synaptic plasticity Sindbis Virus Excitatory Amino Acid Antagonists Neuroscience Ion channel linked receptors |
| Zdroj: | Neuron. 52(5):831-843 |
| ISSN: | 0896-6273 |
| DOI: | 10.1016/j.neuron.2006.10.035 |
| Popis: | Beta amyloid (Abeta), a peptide generated from the amyloid precursor protein (APP) by neurons, is widely believed to underlie the pathophysiology of Alzheimer's disease. Recent studies indicate that this peptide can drive loss of surface AMPA and NMDA type glutamate receptors. We now show that Abeta employs signaling pathways of long-term depression (LTD) to drive endocytosis of synaptic AMPA receptors. Synaptic removal of AMPA receptors is necessary and sufficient to produce loss of dendritic spines and synaptic NMDA responses. Our studies indicate the central role played by AMPA receptor trafficking in Abeta-induced modification of synaptic structure and function. |
| Databáze: | OpenAIRE |
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