Reinsertion or Degradation of AMPA Receptors Determined by Activity-Dependent Endocytic Sorting

Ehlers, Michael D

doi:10.1016/s0896-6273(00)00129-x

Cited by 1,096Neuroscience and Neuropharmacology ResearchCellular transport and secretionReceptor Mechanisms and Signaling

Reinsertion or Degradation of AMPA Receptors Determined by Activity-Dependent Endocytic Sorting

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Ehlers, Michael D·2000·Neuron

DOI 10.1016/s0896-6273(00)00129-x

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Abstract

Both acute and chronic changes in AMPA receptor (AMPAR) localization are critical for synaptic formation, maturation, and plasticity. Here I report that AMPARs are differentially sorted between recycling and degradative pathways following endocytosis. AMPAR sorting occurs in early endosomes and is regulated by synaptic activity and activation of AMPA and NMDA receptors. AMPAR intemalization triggered by NMDAR activation is Ca2+-dependent, requires protein phosphatases, and is followed by rapid membrane reinsertion. Furthermore, NMDAR-mediated AMPAR trafficking is regulated by PKA and accompanied by dephosphorylation and rephosphorylation of GluR1 subunits at a PKA site. In contrast, activation of AMPARs without NMDAR activation targets AMPARs to late endosomes and lysosomes, independent of Ca2+, protein phosphatases, or PKA. These results demonstrate that activity regulates AMPAR endocytic sorting, providing a potential mechanistic link between rapid and chronic changes in synaptic strength.

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In ways that remain to be determined, the increase in CaMKII activity contributes to the insertion of AMPARs.
“In addition, in ways that remain to be determined, the increase in CaMKII activity contributes to the insertion of AMPARs (Ehlers 2000).”
From NMDA receptor-dependent long-term potentiation and long-term depression (LTP/LTD). (2012) · cites this paper as Ehlers 2000
Phosphorylation of AMPAR GluA1 subunits on S845 by PKA increases channel open probability and promotes receptor recycling and exocytosis at extrasynaptic sites near the postsynaptic density.
“Phosphorylation of AMPAR GluA1 (formerly GluR1) subunits on S845 by PKA increases channel open probability and promotes receptor recycling and exocytosis at extrasynaptic sites near the postsynaptic density (PSD)”
From AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors (2012) · cites this paper as Ehlers, 2000
CaN activity is required for cLTD-induced F-actin depolymerization and subsequent disruption of AKAP150 binding to PSD-95 and membranes; this uncoupling may prevent PKA re-phosphorylation of GluA1 that would promote recycling after LTD.
“CaN activity is also required for cLTD-induced F-actin depolymerization and subsequent disruption of AKAP150 binding to PSD-95 and membranes (Gomez et al., 2002); this uncoupling of AKAP150 from PSD-95 and membranes may prevent PKA re-phosphorylation of GluA1 that would promote recycling after LTD”
From AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors (2012) · cites this paper as Ehlers, 2000
PKA activation markedly reduces NMDA (not AMPA)-induced AMPAR endocytosis, whereas PKA inhibition slightly increases NMDA-induced AMPAR endocytosis.
“Consistently, PKA activation markedly reduces NMDA (not AMPA)-induced AMPAR endocytosis, whereas PKA inhibition slightly increases NMDA-induced AMPAR endocytosis [11].”
From Regulated RalBP1 Binding to RalA and PSD-95 Controls AMPA Receptor Endocytosis and LTD (2009) · cites this paper as [11]

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Authors: Ehlers, M. D.
Affiliations: Duke Medical Center (US)
Corresponding author: Ehlers, Michael D
ORCID: Ehlers, Michael D
Venue: Neuron
Publisher: Elsevier BV
Published: 2000-11
Volume: 28
Issue: 2
Pages: 511-525
ISSN: 0896-6273 (ISSN-L)
DOI: 10.1016/s0896-6273(00)00129-x
OpenAlex: W2027436298
Cited by: 1,096
References: 1
Citations by year: 2026: 12 · 2025: 17 · 2024: 20 · 2023: 26 · 2022: 14 · 2021: 35 · 2020: 43 · 2019: 29 · 2018: 40 · 2017: 37 · 2016: 37 · 2015: 39 · 2014: 41 · 2013: 45 · 2012: 39
FWCI: 17.54
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 4641 d)
Locations: Neuron (publishedVersion)
PubMed (publishedVersion)
Funders: National Institute of Neurological Disorders and Stroke (R01 NS39402, R01NS039402)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
Keywords: AMPA receptors, receptor internalization, endocytic sorting, recycling pathway, NMDA receptor activation, protein phosphatase, late endosomes, lysosomes, synaptic plasticity
MeSH terms: Animals, Calcium, Cell Compartmentation, Cell Membrane, Cells, Cultured, Dendrites, Endocytosis, Synaptic Transmission, Neurons, Phosphoprotein Phosphatases, Phosphorylation, Picrotoxin, Endosomes, Synapses, Tetrodotoxin, Receptors, N-Methyl-D-Aspartate, Cyclic AMP-Dependent Protein Kinases, Receptors, AMPA, GABA Antagonists, Protein Transport, Rats

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Reinsertion or Degradation of AMPA Receptors Determined by Activity-Dependent Endocytic Sorting

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