ArticleNeuroscience2008
Dynamic seizure-related changes in extracellular signal-regulated kinase activation in a mouse model of temporal lobe epilepsy.
Article in Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
39 citing papers in PubMed, 62 citations in OpenAlex.
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- Zebrafish models of candidate human epilepsy-associated genes provide evidence of hyperexcitability.iScience · 2024Article
- Use-Dependent, Untapped Dual Kinase Signaling Localized in Brain Learning Circuitry.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Zebrafish models of candidate human epilepsy-associated genes provide evidence of hyperexcitability.bioRxiv : the preprint server for biology · 2024Article
- Dose-dependent seizure control with MEK inhibitor therapy for progressive glioma in a child with neurofibromatosis type 1.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2022Article
- Altered Extracellular Matrix as an Alternative Risk Factor for Epileptogenicity in Brain Tumors.Biomedicines · 2022Review
- Blocking ERK-DAPK1 Axis Attenuates Glutamate Excitotoxicity in Epilepsy.International journal of molecular sciences · 2022Article
- Time and age dependent regulation of neuroinflammation in a rat model of mesial temporal lobe epilepsy: Correlation with human data.Frontiers in cell and developmental biology · 2022Article
- Altered Protein Profiles During Epileptogenesis in the Pilocarpine Mouse Model of Temporal Lobe Epilepsy.Frontiers in neurology · 2021Article
- The Influence of Palmatine Isolated fromCells · 2020Article
- Neurosteroid regulation of GABABrain research · 2019Review
- D-Serine Contributes to Seizure Development via ERK Signaling.Frontiers in neuroscience · 2019Article
- Catalpol Exerts an Anti-Epilepticus Effect, Possibly by Regulating the Nrf2-Keap1-ARE Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Analysis of ERK1/2 kinases in the inferior colliculus of rats genetically prone to audiogenic seizures during postnatal development.Doklady. Biochemistry and biophysics · 2017Article
- SRF modulates seizure occurrence, activity induced gene transcription and hippocampal circuit reorganization in the mouse pilocarpine epilepsy model.Molecular brain · 2017Article
- Effects of pharmacological treatments on hippocampal NCAM1 and ERK2 expression in epileptic rats with cognitive dysfunction.Oncology letters · 2016Article
- Epilepsy, Antiepileptic Drugs, and Aggression: An Evidence-Based Review.Pharmacological reviews · 2016Review
- Sprouty2 and -4 hypomorphism promotes neuronal survival and astrocytosis in a mouse model of kainic acid induced neuronal damage.Hippocampus · 2016Article
- Involvement of BDNF/ERK signaling in spontaneous recovery from trimethyltin-induced hippocampal neurotoxicity in mice.Brain research bulletin · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Extracellular signal-regulated kinase (ERK) is highly sensitive to regulation by neuronal activity and is critically involved in several forms of synaptic plasticity. These features suggested that alterations in ERK signaling might occur in epilepsy. Previous studies have described increased ERK phosphorylation immediately after the induction of severe seizures, but patterns of ERK activation in epileptic animals during the chronic period have not been determined. Thus, the localization and abundance of phosphorylated extracellular signal-regulated kinase (pERK) were examined in a pilocarpine model of recurrent seizures in C57BL/6 mice during the seizure-free period and at short intervals after spontaneous seizures. Immunolabeling of pERK in control animals revealed an abundance of distinctly-labeled neurons within the hippocampal formation. However, in pilocarpine-treated mice during the seizure-free period, the numbers of pERK-labeled neurons were substantially decreased throughout much of the hippocampal formation. Double labeling with a general neuronal marker suggested that the decrease in pERK-labeled neurons was not due primarily to cell loss. The decreased ERK phosphorylation in seizure-prone animals was interpreted as a compensatory response to increased neuronal excitability within the network. Nevertheless, striking increases in pERK labeling occurred at the time of spontaneous seizures and were evident in large populations of neurons at very short intervals (as early as 2 min) after detection of a behavioral seizure. These findings suggest that increased pERK labeling could be one of the earliest immunohistochemical indicators of neurons that are activated at the time of a spontaneous seizure.
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Registered trials
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