ArticleEBioMedicine2019
GSK3β activity alleviates epileptogenesis and limits GluA1 phosphorylation.
Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- The Contribution of HCN Channelopathies in Different Epileptic Syndromes, Mechanisms, Modulators, and Potential Treatment Targets: A Systematic Review.Frontiers in molecular neuroscience · 2022Pooled it
- Ibogalogs induce antiseizure activity in rodents by a mechanism involving 5-HTBiochemical pharmacology · 2026Article
- Upregulation of adenosine AMolecular psychiatry · 2025Article
- Integrated computational approaches for identification of potent pyrazole-based glycogen synthase kinase-3β (GSK-3β) inhibitors: 3D-QSAR, virtual screening, docking, MM/GBSA, EC, MD simulation studies.Molecular diversity · 2025Article
- Adiponectin Receptor Agonist Ameliorates Synaptic Dysfunction in 3xTg Alzheimer's Disease Mouse Model by Activation of AMPK.CNS neuroscience & therapeutics · 2025Article
- Gut microbial metabolite TMAO impairs cognitive function and induces hippocampal synaptic plasticity decline through modulation of GSK-3β activity.Alzheimer's research & therapy · 2025Article
- Identification of plasma exosomal microRNAs and bioinformatics analysis of the microRNA-messenger RNA regulatory pathways in mice with status epilepticus.Cytotechnology · 2025Article
- Exploring the Therapeutic Potential of Baicalin: Mitigating Anxiety and Depression in Epileptic Rats.Combinatorial chemistry & high throughput screening · 2025Article
- Mitochondrion-based organellar therapies for central nervous system diseases.Cell communication and signaling : CCS · 2024Review
- Glutaminase-1 inhibition alleviates senescence of Wharton's jelly-derived mesenchymal stem cells via senolysis.Stem cells translational medicine · 2024Article
- The Neurovascular Unit Dysfunction in the Molecular Mechanisms of Epileptogenesis and Targeted Therapy.Neuroscience bulletin · 2024Review
- Curculigoside Attenuates Endoplasmic Reticulum Stress-Induced Epithelial Cell and Fibroblast Senescence by Regulating the SIRT1-P300 Signaling Pathway.Antioxidants (Basel, Switzerland) · 2024Article
- Rab11 regulates autophagy at dendritic spines in an mTOR- and NMDA-dependent manner.Molecular biology of the cell · 2024Article
- Interplay of epilepsy and long-term potentiation: implications for memory.Frontiers in neuroscience · 2024Review
- Brain glycogen content is increased in the acute and interictal chronic stages of the mouse pilocarpine model of epilepsy.Epilepsia open · 2022Article
- A Genetic Model of Epilepsy with a Partial Alzheimer's Disease-Like Phenotype and Central Insulin Resistance.Molecular neurobiology · 2022Article
- Chloride imbalance in Fragile X syndrome.Frontiers in neuroscience · 2022Article
- Unravelling the Role of Glycogen Synthase Kinase-3 in Alzheimer's Disease-Related Epileptic Seizures.International journal of molecular sciences · 2020Review
- Article
- GSK3β and Tau Protein in Alzheimer's Disease and Epilepsy.Frontiers in cellular neuroscience · 2020Article
Corrections and comments
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Authors and funding
20 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlycogen synthase kinase-3β (GSK3β) is a key regulator of cellular homeostasis. In neurons, GSK3β contributes to the control of neuronal transmission and plasticity, but its role in epilepsy remains to be defined.
methodsBiochemical and electrophysiological methods were used to assess the role of GSK3β in regulating neuronal transmission and epileptogenesis. GSK3β activity was increased genetically in GSK3β[S9A] mice. Its effects on neuronal transmission and epileptogenesis induced by kainic acid were assessed by field potential recordings in mice brain slices and video electroencephalography in vivo. The ion channel expression was measured in brain samples from mice and followed by analysis in samples from patients with temporal lobe epilepsy or focal cortical dysplasia in correlation to GSK3β phosphorylation.
findingsHigher GSK3β activity decreased the progression of kainic acid induced epileptogenesis. At the biochemical level, higher GSK3β activity increased the expression of hyperpolarization-activated cyclic nucleotide-gated (HCN) channel 4 under basal conditions and in the epileptic mouse brain and decreased phosphorylation of the glutamate α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunit GluA1 at Serine 831 under basal conditions. Moreover, we found a significant correlation between higher inhibitory GSK3β phosphorylation at Serine 9 and higher activating GluA1 phosphorylation at Serine 845 in brain samples from epileptic patients.
interpretationOur data imply GSK3β activity in the protection of neuronal networks from hyper-activation in response to epileptogenic stimuli and indicate that the anti-epileptogenic function of GSK3β involves modulation of HCN4 level and the synaptic AMPA receptors pool.
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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.