ArticleEpilepsia2015
Suppressing cAMP response element-binding protein transcription shortens the duration of status epilepticus and decreases the number of spontaneous seizures in the pilocarpine model of epilepsy.
Article in Epilepsia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- Prefrontal TRPM8 Receptor Modulates Epileptic Seizures via PKA/CREB Signaling Pathway in Mice.CNS neuroscience & therapeutics · 2026Article
- Empagliflozin Mitigates PTZ-Induced Seizures in Rats: Modulating Npas4 and CREB-BDNF Signaling Pathway.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Mossy Fiber Sprouting in Temporal Lobe Epilepsy: The Impact of Netrin-1, DCC, and Gene Expression Changes.Biomedicines · 2024Article
- Molecular Genetics of Acquired Temporal Lobe Epilepsy.Biomolecules · 2024Review
- The Role of the Possible Receptors and Intracellular Pathways in Protective Effect of Exogenous Anandamide in Kindling Model of Epilepsy.Neurochemical research · 2022Article
- Article
- Inhibition of AKT/GSK3β/CREB Pathway Improves the Responsiveness to AMPA Receptor Antagonists by Regulating GRIA1 Surface Expression in Chronic Epilepsy Rats.Biomedicines · 2021Article
- PKA-RIIβ autophosphorylation modulates PKA activity and seizure phenotypes in mice.Communications biology · 2021Article
- Deletion of FGF9 in GABAergic neurons causes epilepsy.Cell death & disease · 2021Article
- Src/CK2/PTEN-Mediated GluN2B and CREB Dephosphorylations Regulate the Responsiveness to AMPA Receptor Antagonists in Chronic Epilepsy Rats.International journal of molecular sciences · 2020Article
- [Regulatory mechanism of MS275 on the p38 MAPK signaling pathway in rats with convulsion in the developmental stage].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2020Article
- Aspects of cAMP Signaling in Epileptogenesis and Seizures and Its Potential as Drug Target.Neurochemical research · 2020Review
- Inhibition of Acid Sensing Ion Channel 3 Aggravates Seizures by Regulating NMDAR Function.Neurochemical research · 2018Article
- Increased Expression of Brain-Derived Neurotrophic Factor Transcripts I and VI, cAMP Response Element Binding, and Glucocorticoid Receptor in the Cortex of Patients with Temporal Lobe Epilepsy.Molecular neurobiology · 2018Article
- Exploring the pathogenesis of canine epilepsy using a systems genetics method and implications for anti-epilepsy drug discovery.Oncotarget · 2018Article
- CRTC1 nuclear localization in the hippocampus of the pilocarpine-induced status epilepticus model of temporal lobe epilepsy.Neuroscience · 2016Article
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
objectiveCurrent epilepsy therapies directed at altering the function of neurotransmitter receptors or ion channels, or release of synaptic vesicles fail to prevent seizures in approximately 30% of patients. A better understanding of the molecular mechanism underlying epilepsy is needed to provide new therapeutic targets. The activity of cyclic AMP (cAMP) response element-binding protein (CREB), a major transcription factor promoting CRE-mediated transcription, increases following a prolonged seizure called status epilepticus. It is also increased in the seizure focus of patients with medically intractable focal epilepsy. Herein we explored the effect of acute suppression of CREB activity on status epilepticus and spontaneous seizures in a chronic epilepsy model.
methodsPilocarpine chemoconvulsant was used to induce status epilepticus. To suppress CREB activity, a transgenic mouse line expressing an inducible dominant negative mutant of CREB (CREB(IR) ) with a serine to alanine 133 substitution was used. Status epilepticus and spontaneous seizures of transgenic and wild-type mice were analyzed using video-electroencephalography (EEG) to assess the effect of CREB suppression on seizures.
resultsOur findings indicate that activation of CREB(IR) shortens the duration of status epilepticus. The frequency of spontaneous seizures decreased in mice with chronic epilepsy during CREB(IR) induction; however, the duration of the spontaneous seizures was unchanged. Of interest, we found significantly reduced levels of phospho-CREB Ser133 upon activation of CREB(IR) , supporting prior work suggesting that binding to the CRE site is important for CREB phosphorylation. SIGNIFICANCE: Our results suggest that CRE transcription supports seizure activity both during status epilepticus and in spontaneous seizures. Thus, blocking of CRE transcription is a novel target for the treatment of epilepsy.
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