ArticleFrontiers in cellular neuroscience2014
Elevated activation of CaMKIIα in the CPEB3-knockout hippocampus impairs a specific form of NMDAR-dependent synaptic depotentiation.
Article in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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20 citing papers in PubMed, 34 citations in OpenAlex.
- An Anti-Amyloidogenic Approach to Specifically Block Memory Consolidation in Mice for Therapeutic Intervention.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Role of CPEBs in Learning and Memory.Journal of neurochemistry · 2025Review
- Structural insights into functional regulation of the human CPEB3 prion by an amyloid-forming segment.Structure (London, England : 1993) · 2025Article
- CPEB and translational control by cytoplasmic polyadenylation: impact on synaptic plasticity, learning, and memory.Molecular psychiatry · 2023Review
- CPEB3 low-complexity motif regulates local protein synthesis via protein-protein interactions in neuronal ribonucleoprotein granules.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Conformational dynamics in the disordered region of human CPEB3 linked to memory consolidation.BMC biology · 2022Article
- αCaMKII in the lateral amygdala mediates PTSD-Like behaviors and NMDAR-Dependent LTD.Neurobiology of stress · 2021Article
- CPEB3-dowregulated Nr3c1 mRNA translation confers resilience to developing posttraumatic stress disorder-like behavior in fear-conditioned mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021Article
- Review
- Emotional Stress Induces Structural Plasticity in Bergmann Glial Cells via an AC5-CPEB3-GluA1 Pathway.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- CPEB3 inhibits translation of mRNA targets by localizing them to P bodies.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Mechanism of P2X7 receptor-dependent enhancement of neuromuscular transmission in pannexin 1 knockout mice.Purinergic signalling · 2018Article
- Autophagy is required for human umbilical cord mesenchymal stem cells to improve spatial working memory in APP/PS1 transgenic mouse model.Stem cell research & therapy · 2018Article
- IL-1β impairs retrograde flow of BDNF signaling by attenuating endosome trafficking.Journal of neuroinflammation · 2017Article
- RNA-binding profiles ofProceedings of the National Academy of Sciences of the United States of America · 2016Article
- Phosphoproteomic Analysis Reveals a Novel Mechanism of CaMKIIα Regulation Inversely Induced by Cocaine Memory Extinction versus Reconsolidation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Separate Ionotropic and Metabotropic Glutamate Receptor Functions in Depotentiation vs. LTP: A Distinct Role for Group1 mGluR Subtypes and NMDARs.Frontiers in cellular neuroscience · 2016Article
- Loss of CPEB3 Upregulates MEGF10 to Impair Mosaic Development of ON Starburst Amacrine Cells.Frontiers in molecular neuroscience · 2016Article
- New Phosphospecific Antibody Reveals Isoform-Specific Phosphorylation of CPEB3 Protein.PloS one · 2016Article
- Article
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5 authors at 2 institutions in 1 country.
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Abstract
Cytoplasmic polyadenylation element binding protein 3 (CPEB3) is a sequence-specific RNA-binding protein that confines the strength of glutamatergic synapses by translationally downregulating the expression of multiple plasticity-related proteins (PRPs), including the N-methyl-D-aspartate receptor (NMDAR) and the postsynaptic density protein 95 (PSD95). CPEB3 knockout (KO) mice exhibit hippocampus-dependent abnormalities related not only to long-term spatial memory but also to the short-term acquisition and extinction of contextual fear memory. In this study, we identified a specific form of NMDAR-dependent synaptic depotentiation (DPT) that is impaired in the adult CPEB3 KO hippocampus. In parallel, cultured KO neurons also exhibited delayed morphological and biochemical responses under NMDA-induced chemical long-term depression (c-LTD). The c-LTD defects in the KO neurons include elevated activation of calcium/calmodulin-dependent protein kinase II alpha subunit (CaMKIIα), increased Ser831 phosphorylation of GluA1 and slow degradation of PSD95 and GluA1. Because transient pharmacological suppression of CaMKIIα activity during the DPT-initiating phase successfully reversed the LTP in the KO hippocampus, DPT and c-LTD in the two different systems shared common molecular defects due to the absence of CPEB3. Together, our results suggest that CPEB3 deficiency imbalances NMDAR-activated CaMKIIα signaling, which consequently fails to depress synaptic strength under certain stimulation conditions.
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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.