ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Synaptic stimulation of mTOR is mediated by Wnt signaling and regulation of glycogen synthetase kinase-3.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 75 citations in OpenAlex.
- Osteoarthritis and dementia: contrasting disorders driven by mutual pathways of autophagy, mTOR, GLP-1, AMPK, Wnt, and WISP1.Expert review of clinical pharmacology · 2026Review
- Combinational BET and mTOR inhibition unveils EGR1 as acute myeloid leukemia prognostic biomarker.Scientific reports · 2025Article
- Cell Type-Specific mTORC1 Signaling and Translational Control in Synaptic Plasticity and Memory.Journal of neurochemistry · 2025Review
- Computational modeling of AMPK and mTOR crosstalk in glutamatergic synapse calcium signaling.NPJ systems biology and applications · 2023Article
- Roles of eukaryotic elongation factor 2 kinase (eEF2K) in neuronal plasticity, cognition, and Alzheimer disease.Journal of neurochemistry · 2023Review
- Review
- Targeting CaN/NFAT in Alzheimer's brain degeneration.Frontiers in immunology · 2023Review
- Rescue of deficits by Brwd1 copy number restoration in the Ts65Dn mouse model of Down syndrome.Nature communications · 2022Article
- Circulating hsa-let-7e-5p and hsa-miR-125a-5p as Possible Biomarkers in the Diagnosis of Major Depression and Bipolar Disorders.Disease markers · 2022Article
- The GSK-3β/β-Catenin Signaling-Mediated Brain-Derived Neurotrophic Factor Pathway Is Involved in Aluminum-Induced Impairment of Hippocampal LTP In Vivo.Biological trace element research · 2021Article
- Isoform-specific dysregulation of AMP-activated protein kinase signaling in a non-human primate model of Alzheimer's disease.Neurobiology of disease · 2021Article
- Proteomics of autism and Alzheimer's mouse models reveal common alterations in mTOR signaling pathway.Translational psychiatry · 2021Article
- Brain-specific suppression of AMPKα2 isoform impairs cognition and hippocampal LTP by PERK-mediated eIF2α phosphorylation.Molecular psychiatry · 2021Article
- Review
- Pharmacological and phosphoproteomic approaches to roles of protein kinase C in kappa opioid receptor-mediated effects in mice.Neuropharmacology · 2020Article
- Cell Type- and Stimulation-Dependent Transcriptional Programs Regulated by Atg16L1 and Its Crohn's Disease Risk Variant T300A.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Therapeutic Potential of Glucagon-Like Peptide-1 Cleavage Product for Alzheimer's Disease.Neuroscience bulletin · 2019Review
- Memory Decline and Behavioral Inflexibility in Aged Mice Are Correlated With Dysregulation of Protein Synthesis Capacity.Frontiers in aging neuroscience · 2019Article
- Therapeutic Potential of AMP-Activated Protein Kinase in Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2019Review
- Cortical astroglia undergo transcriptomic dysregulation in the G93A SOD1 ALS mouse model.Journal of neurogenetics · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The persistent or "late" phase of long-term potentiation (L-LTP), which requires protein synthesis, can be induced by relatively intense synaptic activity. The ability of such strong synaptic protocols to engage the translational machinery and produce plasticity-related proteins, while weaker protocols activate only posttranslational processes and transient potentiation (early LTP; E-LTP), is not understood. Among the major translation control pathways in neurons, the stimulation of mammalian target of rapamycin (mTOR) is a key event in the induction of L-LTP. We report that mTOR is tonically suppressed in rat hippocampus under resting conditions, a consequence of the basal activity of glycogen synthetase kinase 3 (GSK3). This suppression could be overcome by weak synaptic stimulation in the presence of the β-adrenergic agonist isoproterenol, a combination that induced L-LTP, and activation of mTOR coincided with the Akt-mediated phosphorylation of GSK3. Surprisingly, while isoproterenol alone elevated Akt activity, it failed to increase GSK3 phosphorylation or mTOR signaling, showing that Akt was uncoupled from these effectors in the absence of synaptic stimulation. With the addition of weak stimulation, Akt signaled to GSK3 and mTOR, a gating effect that was mediated by voltage-dependent Ca(2+) channels and the Wnt pathway. mTOR could be stimulated by pharmacological inhibition, enabling weak HFS to induce L-LTP. These results establish GSK3 as an integrator of Akt and Wnt signals and suggest that overcoming GSK3-mediated suppression of mTOR is a key event in the induction of L-LTP by synaptic activity.
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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.