ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2018
Suppression of AMPA Receptor Exocytosis Contributes to Hippocampal LTD.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 18 citations in OpenAlex.
- Designing Neural Dynamics: From Digital Twin Modeling to Regeneration.International journal of molecular sciences · 2025Review
- Local Iontophoretic Application for Pharmacological Induction of Long-Term Synaptic Depression.Bio-protocol · 2025Article
- The effect of traumatic brain injury on learning and memory: A synaptic focus.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2025Review
- Fluorescence lifetime imaging of AMPA receptor endocytosis in living neurons: effects of Aβ and PP1.Frontiers in molecular neuroscience · 2024Article
- Imaging of post-synaptic membrane trafficking in neuronal dendrites: progress, limitations, and new developments.Neurophotonics · 2023Article
- Activity-Dependent Phosphorylation of CDKL5 at Serine 407 Regulates Synaptogenesis and Plasticity.Neuroscience bulletin · 2023Article
- Live-cell imaging of endocytosed synaptophysin around individual hippocampal presynaptic active zones.Frontiers in cellular neuroscience · 2023Article
- The Shaping of AMPA Receptor Surface Distribution by Neuronal Activity.Frontiers in synaptic neuroscience · 2022Review
- NMDAR-dependent long-term depression is associated with increased short term plasticity through autophagy mediated loss of PSD-95.Nature communications · 2021Article
- NYX-2925 induces metabotropic N-methyl-d-aspartate receptor (NMDAR) signaling that enhances synaptic NMDAR and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor.Journal of neurochemistry · 2020Article
- Changes in Hippocampal Plasticity in Depression and Therapeutic Approaches Influencing These Changes.Neural plasticity · 2020Review
- Inhibitory Receptor Diffusion Dynamics.Frontiers in molecular neuroscience · 2019Article
- Amyloid-β oligomers suppress subunit-specific glutamate receptor increase during LTP.Alzheimer's & dementia (New York, N. Y.) · 2019Article
- Visualization of Exo- and Endocytosis of AMPA Receptors During Hippocampal Synaptic Plasticity Around Postsynaptic-Like Membrane Formed on Glass Surface.Frontiers in cellular neuroscience · 2018Article
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3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The decrease in number of AMPA-type glutamate receptor (AMPAR) at excitatory synapses causes LTD, a cellular basis of learning and memory. The number of postsynaptic AMPARs is regulated by the balance of exocytosis and endocytosis, and enhanced endocytosis of AMPAR has been suggested to underlie the LTD expression. However, it remains unclear how endocytosis and exocytosis of AMPAR change during LTD. In this study, we addressed this question by analyzing exocytosis and endocytosis of AMPAR by imaging super-ecliptic pHlorin (SEP)-tagged AMPAR around postsynaptic structure formed directly on the glass surface in the hippocampal culture prepared from rat embryos of both sexes. Contrary to a prevailing view on the LTD expression by endocytosis enhancement, the LTD induction by NMDA application only transiently enhanced endocytosis of SEP-tagged GluA1 subunits of AMPAR, which was counteracted by simultaneous augmentation of exocytosis. As a result, soon after the start of the LTD induction (∼1 min), the surface AMPAR did not markedly decrease. Thereafter, the surface GluA1-SEP gradually decreased (2-5 min) and kept at a low level until the end of observation (>30 min). Surprisingly, this gradual and sustained decrease of surface AMPAR was accompanied not by the enhanced endocytic events of GluA1, but by the suppression of exocytosis. Together, our data highlight an unprecedented mechanism for the LTD expression by attenuation of exocytosis of AMPAR, but not by enhanced endocytosis, together with a reduction of postsynaptic AMPAR scaffolding protein PSD95.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.