Clathrin-independent trafficking of AMPA receptors

Membrane trafficking of AMPA receptors (AMPARs) is critical for neuronal function and plasticity. Although rapid forms of AMPAR internalization during long-term depression (LTD) require clathrin and dynamin, the mechanisms governing constitutive AMPAR turnover and internalization of AMPARs during sl...

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Published inThe Journal of neuroscience Vol. 35; no. 12; pp. 4830 - 4836
Main Authors Glebov, Oleg O, Tigaret, Cezar M, Mellor, Jack R, Henley, Jeremy M
Format Journal Article
LanguageEnglish
Published United States Society for Neuroscience 25.03.2015
Subjects
Actins - metabolism
Aminoquinolines - pharmacology
Animals
Brief Communications
Cell Culture Techniques
Clathrin - antagonists & inhibitors
Clathrin - metabolism
Dynamins - antagonists & inhibitors
Dynamins - metabolism
Hippocampus - metabolism
Hippocampus - physiology
Hydrazones - pharmacology
Long-Term Synaptic Depression - drug effects
Long-Term Synaptic Depression - physiology
Male
Neurons - drug effects
Neurons - physiology
Protein Transport - drug effects
Protein Transport - physiology
Pyrimidines - pharmacology
rac1 GTP-Binding Protein - antagonists & inhibitors
rac1 GTP-Binding Protein - physiology
Rats
Receptors, AMPA - metabolism
RNA, Small Interfering - pharmacology
endocytosis
AMPA receptors
synaptic plasticity
membrane trafficking
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Summary:Membrane trafficking of AMPA receptors (AMPARs) is critical for neuronal function and plasticity. Although rapid forms of AMPAR internalization during long-term depression (LTD) require clathrin and dynamin, the mechanisms governing constitutive AMPAR turnover and internalization of AMPARs during slow homeostatic forms of synaptic plasticity remain unexplored. Here, we show that, in contrast to LTD, constitutive AMPAR internalization and homeostatic AMPAR downscaling in rat neurons do not require dynamin or clathrin function. Instead, constitutive AMPAR trafficking is blocked by a Rac1 inhibitor and is regulated by a dynamic nonstructural pool of F-actin. Our findings reveal a novel role for neuronal clathrin-independent endocytosis controlled by actin dynamics and suggest that the interplay between different modes of receptor endocytosis provides for segregation between distinct modes of neuronal plasticity.
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Author contributions: O.O.G., J.R.M., and J.M.H. designed research; O.O.G. and C.M.T. performed research; O.O.G., C.M.T., and J.R.M. analyzed data; O.O.G. and J.M.H. wrote the paper.
ISSN:0270-6474
1529-2401
DOI:10.1523/jneurosci.3571-14.2015