ArticleThe Journal of clinical investigation2015
Long-term potentiation decay and memory loss are mediated by AMPAR endocytosis.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.
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Who cites it
99 citing papers in PubMed, 202 citations in OpenAlex.
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- ELK1 inhibition alleviates amyloid pathology and memory decline by promoting the SYVN1-mediated ubiquitination and degradation of PS1 in Alzheimer's disease.Experimental & molecular medicine · 2025Article
- AMPA Receptor Modulation in the Treatment of High-Grade Glioma: Translating Good Science into Better Outcomes.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Amplification of the therapeutic potential of AMPA receptor potentiators from the nootropic era to today.Pharmacology, biochemistry, and behavior · 2025Review
- Stress Molecular Signaling in Interaction With Cognition.Biological psychiatry · 2025Review
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- Coexistence of anti-neurexin-3α-associated autoimmune encephalitis and systemic lupus erythematosus in an adult patient: a case report.Frontiers in immunology · 2025Article
- PKMζ drives spatial memory reconsolidation but not maintenance.Frontiers in synaptic neuroscience · 2025Article
- Resource-dependent heterosynaptic spike-timing-dependent plasticity in recurrent networks with and without synaptic degeneration.Frontiers in computational neuroscience · 2025Article
- Endogenous Recovery of Hippocampal Function Following Global Cerebral Ischemia in Juvenile Female Mice Is Influenced by Neuroinflammation and Circulating Sex Hormones.Neural plasticity · 2025Article
- A small molecule p38α MAPK inhibitor, MW150, attenuates behavioral deficits and neuronal dysfunction in a mouse model of mixed amyloid and vascular pathologies.Brain, behavior, & immunity - health · 2024Article
- Active forgetting and neuropsychiatric diseases.Molecular psychiatry · 2024Review
- Slow-wave sleep drives sleep-dependent renormalization of synaptic AMPA receptor levels in the hypothalamus.PLoS biology · 2024Article
- KIBRA anchoring the action of PKMζ maintains the persistence of memory.Science advances · 2024Article
- Uric Acid Mitigates Cognitive Deficits via TFEB-Mediated Microglial Autophagy in Mice Models of Alzheimer's Disease.Molecular neurobiology · 2024Article
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- Photobiomodulation in experimental models of Alzheimer's disease: state-of-the-art and translational perspectives.Alzheimer's research & therapy · 2024Review
- Haplotype-resolved and chromosome-scale genomes provide insights into co-adaptation between the Amur tiger and Amur leopard.Zoological research · 2024Article
39 more citing papers are in PubMed but not listed here.
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Authors and funding
20 authors at 3 institutions in 2 countries.
Funding
Abstract
Long-term potentiation (LTP) of synaptic strength between hippocampal neurons is associated with learning and memory, and LTP dysfunction is thought to underlie memory loss. LTP can be temporally and mechanistically classified into decaying (early-phase) LTP and nondecaying (late-phase) LTP. While the nondecaying nature of LTP is thought to depend on protein synthesis and contribute to memory maintenance, little is known about the mechanisms and roles of decaying LTP. Here, we demonstrated that inhibiting endocytosis of postsynaptic α-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptors (AMPARs) prevents LTP decay, thereby converting it into nondecaying LTP. Conversely, restoration of AMPAR endocytosis by inhibiting protein kinase Mζ (PKMζ) converted nondecaying LTP into decaying LTP. Similarly, inhibition of AMPAR endocytosis prolonged memory retention in normal animals and reduced memory loss in a murine model of Alzheimer's disease. These results strongly suggest that an active process that involves AMPAR endocytosis mediates the decay of LTP and that inhibition of this process can prolong the longevity of LTP as well as memory under both physiological and pathological conditions.
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Registered trials
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.