ArticleEpilepsia2012
Reduction in delayed mortality and subtle improvement in retrograde memory performance in pilocarpine-treated mice with conditional neuronal deletion of cyclooxygenase-2 gene.
Article in Epilepsia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- Circular RNA PTPN4 Contributes to Blood-Brain Barrier Disruption during Early Epileptogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Neuroinflammation and Disease: Pathways and Opportunities.Annual review of pharmacology and toxicology · 2026Review
- Brain-invading monocytes promote seizure-associated cognitive deficits and neurodegeneration.Neuropharmacology · 2025Article
- Modulating inflammatory prostaglandin E2 signaling to mitigate neurobehavioral comorbidities associated with seizure disorders.Acta pharmaceutica Sinica. B · 2025Review
- Nedl1 knockout ameliorates cognitive impairment and improves epilepsy threshold in pilocarpine-induced epileptic mice.Acta epileptologica · 2025Article
- A Narrative Review of the Published Pre-Clinical Evaluations: Multiple Effects of Arachidonic Acid, its Metabolic Enzymes and Metabolites in Epilepsy.Molecular neurobiology · 2025Review
- Preclinical development of an EP2 antagonist for post-seizure cognitive deficits.Neuropharmacology · 2023Article
- Peripheral Myeloid Cell EP2 Activation Contributes to the Deleterious Consequences of Status Epilepticus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Targeting prostaglandin receptor EP2 for adjunctive treatment of status epilepticus.Pharmacology & therapeutics · 2020Review
- Early treatment with C1 esterase inhibitor improves weight but not memory deficits in a rat model of status epilepticus.Physiology & behavior · 2019Article
- G protein-coupled receptors in acquired epilepsy: Druggability and translatability.Progress in neurobiology · 2019Review
- Suppressing pro-inflammatory prostaglandin signaling attenuates excitotoxicity-associated neuronal inflammation and injury.Neuropharmacology · 2019Article
- The COX-2/prostanoid signaling cascades in seizure disorders.Expert opinion on therapeutic targets · 2019Review
- Infiltrating monocytes promote brain inflammation and exacerbate neuronal damage after status epilepticus.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Anti-Inflammatory Small Molecules To Treat Seizures and Epilepsy: From Bench to Bedside.Trends in pharmacological sciences · 2016Review
- Conditional Disabled-1 Deletion in Mice Alters Hippocampal Neurogenesis and Reduces Seizure Threshold.Frontiers in neuroscience · 2016Article
- Contribution of protease-activated receptor 1 in status epilepticus-induced epileptogenesis.Neurobiology of disease · 2015Article
- Therapeutic window for cyclooxygenase-2 related anti-inflammatory therapy after status epilepticus.Neurobiology of disease · 2015Article
- Co-administration of subtherapeutic diazepam enhances neuroprotective effect of COX-2 inhibitor, NS-398, after lithium pilocarpine-induced status epilepticus.Neuroscience · 2015Article
- Indomethacin can downregulate the levels of inflammatory mediators in the hippocampus of rats submitted to pilocarpine-induced status epilepticus.Clinics (Sao Paulo, Brazil) · 2014Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
purposePilocarpine induces prolonged status epilepticus (SE) in rodents that results in neurodegeneration and cognitive deficits, both commonly observed to be associated with human temporal lobe epilepsy. The multifunctional neuronal modulator, cyclooxygenase-2 (PTGS2 or COX-2), is rapidly induced after SE, mainly in principal neurons of the hippocampal formation and cortex. We used mice in which COX-2 is conditionally ablated in principal forebrain neurons to investigate the involvement of neuron-derived COX-2 in delayed mortality and performance in the Barnes maze.
methodsUsing the COX-2 conditional knockout mouse (nCOX-2 cKO) and their littermate wild-type controls, we compared motor behavior and performance in the Barnes maze before and 3 weeks after the induction of SE by pilocarpine. Mortality rate was also measured during SE and in the week following SE. KEY
findingsnCOX-2 cKO mice showed less delayed mortality than wild-type mice in the week after SE. Although motor behavior and most cognitive measures were not different in the nCOX-2 cKO, upon reexposure to the maze 3 weeks after pilocarpine, the latency to find the previously learned target hole was significantly shorter in the nCOX-2 cKO than their wild-type littermate controls. By this measure pilocarpine-treated nCOX-2 cKO mice were identical to mice that had not experienced SE. SIGNIFICANCE: Results point to a role for neuronal COX-2 in delayed mortality in mice during the week following SE and suggest that neuronal COX-2 contributes to selected cognitive deficits observed after SE. Taking into consideration our previous findings that neurodegeneration and neuroinflammation after SE are reduced in the nCOX-2 cKO, and opening of the blood-brain barrier after pilocarpine is prevented, we conclude that neuronal COX-2 induction is an early step in many of the deleterious consequences of SE.
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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.