ArticleNeural plasticity2016
Seizure-Induced Regulations of Amyloid-β, STEP61, and STEP61 Substrates Involved in Hippocampal Synaptic Plasticity.
Article in Neural plasticity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Neuromodulation in new-onset refractory status epilepticus.Frontiers in neurology · 2023Pooled it
- Exploration of Canarium odontophyllum fruit phytoconstituents as potential candidates against epilepsy using in silico studies.Journal, genetic engineering & biotechnology · 2025Article
- Neurodegeneration and the immune system: lessons from autoimmune encephalitis.Journal of neurology · 2025Review
- Neuromodulation Techniques in Children with Super-Refractory Status Epilepticus.Brain sciences · 2023Review
- Uncovering the Significance of STEP61 in Alzheimer's Disease: Structure, Substrates, and Interactome.Cellular and molecular neurobiology · 2023Review
- Protein profiling and assessment of amyloid beta levels in plasma in canine refractory epilepsy.Frontiers in veterinary science · 2023Article
- Intraneuronal accumulation of amyloid-β peptides as the pathomechanism linking autism and its co-morbidities: epilepsy and self-injurious behavior - the hypothesis.Frontiers in molecular neuroscience · 2023Article
- Dl-3-n-butylphthalide alleviates cognitive impairment in amyloid precursor protein/presenilin 1 transgenic mice by regulating the striatal-enriched protein tyrosine phosphatase/ERK/cAMP-response element-binding protein signaling pathway.Experimental and therapeutic medicine · 2022Article
- Pharmacological inhibition of STriatal-Enriched protein tyrosine Phosphatase by TC-2153 reduces hippocampal excitability and seizure propensity.Epilepsia · 2022Article
- The role of mTORC1 activation in seizure-induced exacerbation of Alzheimer's disease.Brain : a journal of neurology · 2022Article
- Temporal Lobe Epilepsy and Alzheimer's Disease: From Preclinical to Clinical Evidence of a Strong Association.Journal of Alzheimer's disease reports · 2021Review
- Alzheimer-like amyloid and tau alterations associated with cognitive deficit in temporal lobe epilepsy.Brain : a journal of neurology · 2020Article
- Disruption of Striatal-Enriched Protein Tyrosine Phosphatase Signaling Might Contribute to Memory Impairment in a Mouse Model of Sepsis-Associated Encephalopathy.Neurochemical research · 2019Article
- Prolonged seizure activity causes caspase dependent cleavage and dysfunction of G-protein activated inwardly rectifying potassium channels.Scientific reports · 2017Article
- How Electroconvulsive Therapy Works?: Understanding the Neurobiological Mechanisms.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2017Review
- Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins.Journal of visualized experiments : JoVE · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive cognitive decline. Pathologic accumulation of soluble amyloid-β (Aβ) oligomers impairs synaptic plasticity and causes epileptic seizures, both of which contribute to cognitive dysfunction in AD. However, whether seizures could regulate Aβ-induced synaptic weakening remains unclear. Here we show that a single episode of electroconvulsive seizures (ECS) increased protein expression of membrane-associated STriatal-Enriched protein tyrosine Phosphatase (STEP61) and decreased tyrosine-phosphorylation of its substrates N-methyl D-aspartate receptor (NMDAR) subunit GluN2B and extracellular signal regulated kinase 1/2 (ERK1/2) in the rat hippocampus at 2 days following a single ECS. Interestingly, a significant decrease in ERK1/2 expression and an increase in APP and Aβ levels were observed at 3-4 days following a single ECS when STEP61 level returned to the baseline. Given that pathologic levels of Aβ increase STEP61 activity and STEP61-mediated dephosphorylation of GluN2B and ERK1/2 leads to NMDAR internalization and ERK1/2 inactivation, we propose that upregulation of STEP61 and downregulation of GluN2B and ERK1/2 phosphorylation mediate compensatory weakening of synaptic strength in response to acute enhancement of hippocampal network activity, whereas delayed decrease in ERK1/2 expression and increase in APP and Aβ expression may contribute to the maintenance of this synaptic weakening.
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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.