ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999
Persistent increased DNA-binding and expression of serum response factor occur with epilepsy-associated long-term plasticity changes.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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Who cites it
15 citing papers in PubMed, 42 citations in OpenAlex.
- Molecular Genetics of Acquired Temporal Lobe Epilepsy.Biomolecules · 2024Review
- Impaired Glutamate Receptor Function Underlies Early Activity Loss of Ipsilesional Motor Cortex after Closed-Head Mild Traumatic Brain Injury.Journal of neurotrauma · 2021Article
- SRF modulates seizure occurrence, activity induced gene transcription and hippocampal circuit reorganization in the mouse pilocarpine epilepsy model.Molecular brain · 2017Article
- Adult Deletion of SRF Increases Epileptogenesis and Decreases Activity-Induced Gene Expression.Molecular neurobiology · 2016Article
- Overexpression of Serum Response Factor in Neurons Restores Ocular Dominance Plasticity in a Model of Fetal Alcohol Spectrum Disorders.Alcoholism, clinical and experimental research · 2015Article
- Antioxidants as a preventive treatment for epileptic process: a review of the current status.Current neuropharmacology · 2014Article
- The role of reactive species in epileptogenesis and influence of antiepileptic drug therapy on oxidative stress.Current neuropharmacology · 2012Article
- Article
- Serum response factor mediated gene activity in physiological and pathological processes of neuronal motility.Frontiers in molecular neuroscience · 2011Article
- Overexpression of serum response factor restores ocular dominance plasticity in a model of fetal alcohol spectrum disorders.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Traumatic brain injury causes a long-lasting calcium (Ca2+)-plateau of elevated intracellular Ca levels and altered Ca2+ homeostatic mechanisms in hippocampal neurons surviving brain injury.The European journal of neuroscience · 2008Article
- Increased neuronal nuclear calcium influx in neonatal seizures.Neurochemical research · 2006Article
- Role of megakaryoblastic acute leukemia-1 in ERK1/2-dependent stimulation of serum response factor-driven transcription by BDNF or increased synaptic activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Cellular mechanisms underlying acquired epilepsy: the calcium hypothesis of the induction and maintainance of epilepsy.Pharmacology & therapeutics · 2005Review
- Evidence that injury-induced changes in hippocampal neuronal calcium dynamics during epileptogenesis cause acquired epilepsy.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
We have previously shown that NMDA receptor activation during status epilepticus (SE) is required to produce epilepsy in in vitro and in vivo models. As in human symptomatic epilepsy, the epilepsy in these models is permanent, suggesting that the pathological activation of NMDA receptors causes permanent plasticity changes in the brain. Ca(2+) influx through NMDA receptors is known to transiently activate a key transcription factor, serum response factor (SRF). Thus, we investigated whether this factor, in terms of its expression and ability to bind to the consensus serum response element, was altered long term in the pilocarpine model of epilepsy. In hippocampal nuclear extracts, SRF binding to DNA was significantly increased over saline-injected control rats at 24 hr and at 8 weeks after the onset of SE. This increase was shown to be the result of significantly elevated levels of SRF. DNA binding was also persistently increased in the cortical, but not in the cerebellar, extracts. Hippocampal expression of SRF was localized to neurons using immunohistochemistry. NMDA receptor activation during SE was required for these changes to take place, and the spontaneous seizures seen in epileptic rats did not appear to be responsible for the increase in SRF. The results demonstrate that SRF is persistently elevated after SE in the pilocarpine model of epilepsy and support the theory that long-term gene changes in this model occur and are associated with the long-lasting plasticity changes that are initiated during epileptogenesis.
Indexed as
Identifiers
10493724PMC6783053W2152801139What OpenQuestion holds
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.