ArticleNeurotoxicology2010
Soman increases neuronal COX-2 levels: possible link between seizures and protracted neuronal damage.
Article in Neurotoxicology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 44 citations in OpenAlex.
- Spatiotemporal perturbations of the plasminogen activation system in a rat model of acute organophosphate intoxication.Acta neuropathologica communications · 2025Article
- Evidence Implicating Blood-Brain Barrier Impairment in the Pathogenesis of Acquired Epilepsy following Acute Organophosphate Intoxication.The Journal of pharmacology and experimental therapeutics · 2024Review
- Chronic Epilepsy and Mossy Fiber Sprouting Following Organophosphate-Induced Status Epilepticus in Rats.The Journal of pharmacology and experimental therapeutics · 2024Article
- A Novel Second-Generation EP2 Receptor Antagonist Reduces Neuroinflammation and Gliosis After Status Epilepticus in Rats.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- Comparison of neuropathology in rats following status epilepticus induced by diisopropylfluorophosphate and soman.Neurotoxicology · 2021Article
- Neuroinflammation as a Therapeutic Target for Mitigating the Long-Term Consequences of Acute Organophosphate Intoxication.Frontiers in pharmacology · 2021Review
- Urethane attenuates early neuropathology of diisopropylfluorophosphate-induced status epilepticus in rats.Neurobiology of disease · 2020Article
- Pre- and postnatal exposure to glyphosate-based herbicide causes behavioral and cognitive impairments in adult mice: evidence of cortical ad hippocampal dysfunction.Archives of toxicology · 2020Article
- A rat model of organophosphate-induced status epilepticus and the beneficial effects of EP2 receptor inhibition.Neurobiology of disease · 2020Review
- Environmental neurotoxicant-induced dopaminergic neurodegeneration: a potential link to impaired neuroinflammatory mechanisms.Pharmacology & therapeutics · 2019Review
- Persistent neuroinflammation and cognitive impairment in a rat model of acute diisopropylfluorophosphate intoxication.Journal of neuroinflammation · 2016Article
- Corticosterone primes the neuroinflammatory response to DFP in mice: potential animal model of Gulf War Illness.Journal of neurochemistry · 2015Article
- Inhibition of the prostaglandin EP2 receptor is neuroprotective and accelerates functional recovery in a rat model of organophosphorus induced status epilepticus.Neuropharmacology · 2015Article
- The role of glutamate and the immune system in organophosphate-induced CNS damage.Neurotoxicity research · 2013Review
- A review of experimental evidence linking neurotoxic organophosphorus compounds and inflammation.Neurotoxicology · 2012Review
- Recent advances in the treatment of organophosphorous poisonings.Iranian journal of medical sciences · 2012Article
- A mouse model of human repetitive mild traumatic brain injury.Journal of neuroscience methods · 2012Article
- [+]-Huperzine A protects against soman toxicity in guinea pigs.Neurochemical research · 2011Article
- Transcriptional responses of the nerve agent-sensitive brain regions amygdala, hippocampus, piriform cortex, septum, and thalamus following exposure to the organophosphonate anticholinesterase sarin.Journal of neuroinflammation · 2011Article
- Transcriptional analysis of rat piriform cortex following exposure to the organophosphonate anticholinesterase sarin and induction of seizures.Journal of neuroinflammation · 2011Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Nerve agent-induced seizures cause neuronal damage in brain limbic and cortical circuits leading to persistent behavioral and cognitive deficits. Without aggressive anticholinergic and benzodiazepine therapy, seizures can be prolonged and neuronal damage progresses for extended periods of time. The objective of this study was to determine the effects of the nerve agent soman on expression of cyclooxygenase-2 (COX-2), the initial enzyme in the biosynthetic pathway of the proinflammatory prostaglandins and a factor that has been implicated in seizure initiation and propagation. Rats were exposed to a toxic dose of soman and scored behaviorally for seizure intensity. Expression of COX-2 was determined throughout brain from 4h to 7 days after exposure by immunohistochemistry and immunoblotting. Microglial activation and astrogliosis were assessed microscopically over the same time-course. Soman increased COX-2 expression in brain regions known to be damaged by nerve agents (e.g., hippocampus, amygdala, piriform cortex and thalamus). COX-2 expression was induced in neurons, and not in microglia or astrocytes, and remained elevated through 7 days. The magnitude of COX-2 induction was correlated with seizure intensity. COX-1 expression was not changed by soman. Increased expression of neuronal COX-2 by soman is a late-developing response relative to other signs of acute physiological distress caused by nerve agents. COX-2-mediated production of prostaglandins is a consequence of the seizure-induced neuronal damage, even after survival of the initial cholinergic crisis is assured. COX-2 inhibitors should be considered as adjunct therapy in nerve agent poisoning to minimize nerve agent-induced seizure activity.
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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.