ArticleThe Journal of pharmacology and experimental therapeutics2011
The GluK1 (GluR5) Kainate/{alpha}-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor antagonist LY293558 reduces soman-induced seizures and neuropathology.
Article in The Journal of pharmacology and experimental therapeutics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 71 citations in OpenAlex.
- Article
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- Acute Paraoxon-Induced Neurotoxicity in a Mouse Survival Model: Oxidative Stress, Dopaminergic System Alterations and Memory Deficits.International journal of molecular sciences · 2024Article
- Preventing Long-Term Brain Damage by Nerve Agent-Induced Status Epilepticus in Rat Models Applicable to Infants: Significant Neuroprotection by Tezampanel Combined with Caramiphen but Not by Midazolam Treatment.The Journal of pharmacology and experimental therapeutics · 2024Article
- Disease-modifying effects of a glial-targeted inducible nitric oxide synthase inhibitor (1400W) in mixed-sex cohorts of a rat soman (GD) model of epilepsy.Journal of neuroinflammation · 2023Article
- Disease-Modifying Effects of a Glial-targeted Inducible Nitric Oxide Synthase Inhibitor (1400W) in Mixed-sex Cohorts of a Rat Soman (GD) Model of Epilepsy.Research square · 2023Article
- Delayed tezampanel and caramiphen treatment but not midazolam protects against long-term neuropathology after soman exposure.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- The Role of Glutamate Receptors in Epilepsy.Biomedicines · 2023Review
- Kainate Receptor Antagonists: Recent Advances and Therapeutic Perspective.International journal of molecular sciences · 2023Review
- Delving into the significance of the His289Tyr single-nucleotide polymorphism in the glutamate ionotropic receptor kainate-1 (Frontiers in molecular neuroscience · 2023Article
- GABAergic circuits of the basolateral amygdala and generation of anxiety after traumatic brain injury.Amino acids · 2022Review
- Article
- A rapidFrontiers in cellular neuroscience · 2022Article
- Structure, Function, and Regulation of the Kainate Receptor.Sub-cellular biochemistry · 2022Review
- Comparative profile of refractory status epilepticus models following exposure of cholinergic agents pilocarpine, DFP, and soman.Neuropharmacology · 2021Article
- Comparison of neuropathology in rats following status epilepticus induced by diisopropylfluorophosphate and soman.Neurotoxicology · 2021Article
- Targeting Ionotropic Glutamate Receptors in the Treatment of Epilepsy.Current neuropharmacology · 2021Review
- Ionotropic Glutamate Receptors in Epilepsy: A Review Focusing on AMPA and NMDA Receptors.Biomolecules · 2020Review
- Soman-induced status epilepticus, epileptogenesis, and neuropathology in carboxylesterase knockout mice treated with midazolam.Epilepsia · 2018Article
- Midazolam-Resistant Seizures and Brain Injury after Acute Intoxication of Diisopropylfluorophosphate, an Organophosphate Pesticide and Surrogate for Nerve Agents.The Journal of pharmacology and experimental therapeutics · 2018Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
The possibility of mass exposure to nerve agents by a terrorist attack necessitates the availability of antidotes that can be effective against nerve agent toxicity even when administered at a relatively long latency after exposure, because medical assistance may not be immediately available. Nerve agents induce status epilepticus (SE), which can cause brain damage or death. Antagonists of kainate receptors that contain the GluK1 (formerly known as GluR5) subunit (GluK1Rs) are emerging as a new potential treatment for SE and epilepsy from animal research, whereas clinical trials to treat pain have shown that the GluK1/α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor antagonist LY293558 [(3S,4aR,6R,8aR)-6-[2-(1(2)H-tetrazole-5-yl)ethyl]decahydroisoquinoline-3-carboxylic acid] is safe and well tolerated. Therefore, we tested whether LY293558 is effective against soman-induced seizures and neuropathology, when administered 1 h after soman exposure, in rats. LY293558 stopped seizures induced by soman and reduced the total duration of SE, monitored by electroencephalographic recordings within a 24 h-period after exposure. In addition, LY293558 prevented neuronal loss in the basolateral amygdala (BLA) and the CA1 hippocampal area on both days 1 and 7 after soman exposure and reduced neuronal degeneration in the CA1, CA3, and hilar hippocampal regions, entorhinal cortex, amygdala, and neocortex on day 1 after exposure and in the CA1, CA3, amygdala, and neocortex on day 7 after exposure. It also prevented the delayed loss of glutamic acid decarboxylase-67 immuno-stained BLA interneurons on day 7 after exposure. LY293558 is a potential new emergency treatment for nerve agent exposure that can be expected to be effective against seizures and brain damage even with late administration.
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