ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Phosphorylation of histone H2A.X as an early marker of neuronal endangerment following seizures in the adult rat brain.
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 27 papers.
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Who cites it
27 citing papers in PubMed, 46 citations in OpenAlex.
- Histone variants: expanding the epigenetic potential of neurons one amino acid at a time.Trends in biochemical sciences · 2025Review
- Novel Techniques for Mapping DNA Damage and Repair in the Brain.International journal of molecular sciences · 2024Review
- Fatal Epileptic Seizures in Mice Having Compromised Glutathione and Ascorbic Acid Biosynthesis.Antioxidants (Basel, Switzerland) · 2023Article
- Oxidative-Stress-Associated Proteostasis Disturbances and Increased DNA Damage in the Hippocampal Granule Cells of the Ts65Dn Model of Down Syndrome.Antioxidants (Basel, Switzerland) · 2022Article
- The threat of programmed DNA damage to neuronal genome integrity and plasticity.Nature genetics · 2022Review
- The Phosphorylated Form of the Histone H2AX (γH2AX) in the Brain from Embryonic Life to Old Age.Molecules (Basel, Switzerland) · 2021Review
- Article
- Neuronal Cell Cycle Re-Entry Enhances Neuropathological Features in AppNLF Knock-In Mice.Journal of Alzheimer's disease : JAD · 2021Article
- Profiling DNA break sites and transcriptional changes in response to contextual fear learning.PloS one · 2021Article
- Nuclear WRAP53 promotes neuronal survival and functional recovery after stroke.Science advances · 2020Article
- The role of adenosine in epilepsy.Brain research bulletin · 2019Review
- Activity-Induced Regulation of Synaptic Strength through the Chromatin Reader L3mbtl1.Cell reports · 2018Article
- Tau exacerbates excitotoxic brain damage in an animal model of stroke.Nature communications · 2017Article
- Anesthetic Isoflurane Induces DNA Damage Through Oxidative Stress and p53 Pathway.Molecular neurobiology · 2017Article
- Glutamate Induces Blood-Brain Barrier Permeability through Activation of N-Methyl-D-Aspartate Receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Lithium promotes DNA stability and survival of ischemic retinal neurocytes by upregulating DNA ligase IV.Cell death & disease · 2016Article
- Identification and Characterization of New Chemical Entities Targeting Apurinic/Apyrimidinic Endonuclease 1 for the Prevention of Chemotherapy-Induced Peripheral Neuropathy.The Journal of pharmacology and experimental therapeutics · 2016Article
- Long-term window of ischemic tolerance: An evolutionarily conserved form of metabolic plasticity regulated by epigenetic modifications?Journal of neurology & neuromedicine · 2016Article
- Epigenetics and Epilepsy.Cold Spring Harbor perspectives in medicine · 2015Review
- Novel para-phenyl substituted diindolylmethanes protect against MPTP neurotoxicity and suppress glial activation in a mouse model of Parkinson's disease.Toxicological sciences : an official journal of the Society of Toxicology · 2015Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The phosphorylated form of histone H2A.X (γ-H2AX) is a well documented early, sensitive, and selective marker of DNA double-strand breaks (DSBs). Previously, we found that excessive glutamatergic activity increased γ-H2AX in neurons in vitro. Here, we evaluated γ-H2AX formation in the adult rat brain following neuronal excitation evoked by seizure activity in vivo. We found that brief, repeated electroconvulsive shock (ECS)-induced seizures (three individual seizures within 60 min) did not trigger an increase γ-H2AX immunostaining. In contrast, a cluster of 5-7 individual seizures evoked by kainic acid (KA) rapidly (within 30 min) induced γ-H2AX in multiple neuronal populations in hippocampus and entorhinal cortex. This duration of seizure activity is well below threshold for induction of neuronal cell death, indicating that the γ-H2AX increase occurs in response to sublethal insults. Moreover, an increase in γ-H2AX was seen in dentate granule cells, which are resistant to cell death caused by KA-evoked seizures. With as little as a 5 min duration of status epilepticus (SE), γ-H2AX increased in CA1, CA3, and entorhinal cortex to a greater extent than that observed after the clusters of individual seizures, with still greater increases after 120 min of SE. Our findings provide the first direct demonstration that DNA DSB damage occurs in vivo in the brain following seizures. Furthermore, we found that the γ-H2AX increase caused by 120 min of SE was prevented by neuroprotective preconditioning with ECS-evoked seizures. This demonstrates that DNA DSB damage is an especially sensitive indicator of neuronal endangerment and that it is responsive to neuroprotective intervention.
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Registered trials
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