ArticleNeurotoxicology2008
NMDA-induced seizure intensity is enhanced in COX-2 deficient mice.
Article in Neurotoxicology, 2008. 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, 42 citations in OpenAlex.
- Edaravone Modulates NLRP3 Inflammasome Component Expression and Attenuates Glial Cell Morphological Alterations After Status epilepticus.Journal of molecular neuroscience : MN · 2025Article
- PLPP/CIN-mediated NF2 S10 dephosphorylation distinctly regulates kainate-induced seizure susceptibility and neuronal death through PAK1-NF-κB-COX-2-PTGES2 signaling pathway.Journal of neuroinflammation · 2023Article
- Comparison of three administration modes for establishing a zebrafish seizure model induced by N-Methyl-D-aspartic acid.World journal of psychiatry · 2020Article
- Edaravone acts as a potential therapeutic drug against pentylenetetrazole-induced epilepsy in male albino rats by downregulating cyclooxygenase-II.Brain and behavior · 2019Article
- Applications for α-lactalbumin in human nutrition.Nutrition reviews · 2018Review
- Novel therapeutic approaches for disease-modification of epileptogenesis for curing epilepsy.Biochimica et biophysica acta. Molecular basis of disease · 2017Review
- Animal Models of Posttraumatic Seizures and Epilepsy.Methods in molecular biology (Clifton, N.J.) · 2016Article
- The role of inflammation in epileptogenesis.Neuropharmacology · 2013Review
- Immune mechanisms in epileptogenesis.Frontiers in cellular neuroscience · 2013Review
- Article
- Neuromodulatory role of endogenous interleukin-1β in acute seizures: possible contribution of cyclooxygenase-2.Neurobiology of disease · 2012Article
- Ablation of cyclooxygenase-2 in forebrain neurons is neuroprotective and dampens brain inflammation after status epilepticus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Neuroprotective role of PrPC against kainate-induced epileptic seizures and cell death depends on the modulation of JNK3 activation by GluR6/7-PSD-95 binding.Molecular biology of the cell · 2011Article
- Review
- Prophylactic, prandial rofecoxib treatment lacks efficacy against acute PTZ-induced seizure generation and kindling acquisition.Epilepsia · 2011Article
- Cyclooxygenase-1 and -2 differentially modulate lipopolysaccharide-induced blood-brain barrier disruption through matrix metalloproteinase activity.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2010Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Pharmacological inhibition or genetic deletion of cyclooxygenase (COX)-2, but not COX-1, has been shown to increase susceptibility to kainic acid (KA)-induced excitotoxicity. However, it is unclear if susceptibility to excitotoxins that act through other neurotransmitter receptors is altered by COX-2 inhibition. To further understand the involvement of COX-2 in regulating susceptibility to excitotoxicity, we investigated the effect of COX-2 deletion on excitotoxicity induced by peripheral injection of N-methyl-d-aspartate (NMDA, a specific agonist of the NMDA receptors) or lindane (a GABA(A) receptor antagonist). COX-2(-/-) mice injected intraperitoneally with NMDA (50-100mg/kg) exhibited significantly increased median seizure intensity when compared to COX-2(+/+) mice. Further, COX-2(-/-) mice exposed to NMDA showed neuronal damage, detected by Fluoro Jade B (FJB) staining, in the CA3 region of the hippocampus. There was no FJB staining nor any significant difference in median or maximal seizure intensity in COX-2(+/+) and COX-2(-/-) mice exposed to lindane. LC-MS/MS analysis of brain prostaglandin profile in COX-2(-/-) mice demonstrated a significant increase in PGF(2alpha), TXB(2), PGE(2) and PGD(2) expression 1h after administration of an excitotoxic dose of KA, but not of NMDA. Our findings demonstrate that COX-2 regulates susceptibility to KA and NMDA excitotoxicity, which directly activate glutamatergic neurotransmission, but not to lindane, which indirectly alters glutamatergic neurotransmission. Furthermore, increased levels of prostaglandins after seizures are associated with consistent manifestation of neuronal damage.
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