ArticleNeuropharmacology2015
LY293558 prevents soman-induced pathophysiological alterations in the basolateral amygdala and the development of anxiety.
Article in Neuropharmacology, 2015. 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, 27 citations in OpenAlex.
- Mitigating organophosphate nerve agent, soman (GD), induced long-term neurotoxicity: Saracatinib, a Src Tyrosine Kinase inhibitor, as a potential countermeasure.Journal of neuroinflammation · 2025Article
- 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
- Sex-based structural and functional MRI outcomes in the rat brain after soman (GD) exposure-induced status epilepticus.Epilepsia open · 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
- Treatment of cholinergic-induced status epilepticus with polytherapy targeting GABA and glutamate receptors.Epilepsia open · 2023Review
- Delayed tezampanel and caramiphen treatment but not midazolam protects against long-term neuropathology after soman exposure.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- Article
- TRPV4 Regulates Soman-Induced Status Epilepticus and Secondary Brain Injury via NMDA Receptor and NLRP3 Inflammasome.Neuroscience bulletin · 2021Article
- A rat model of organophosphate-induced status epilepticus and the beneficial effects of EP2 receptor inhibition.Neurobiology of disease · 2020Review
- Full Protection Against Soman-Induced Seizures and Brain Damage by LY293558 and Caramiphen Combination Treatment in Adult Rats.Neurotoxicity research · 2018Article
- Comparing the Antiseizure and Neuroprotective Efficacy of LY293558, Diazepam, Caramiphen, and LY293558-Caramiphen Combination against Soman in a Rat Model Relevant to the Pediatric Population.The Journal of pharmacology and experimental therapeutics · 2018Article
- Susceptibility to Soman Toxicity and Efficacy of LY293558 Against Soman-Induced Seizures and Neuropathology in 10-Month-Old Male Rats.Neurotoxicity research · 2017Article
- Paraoxon: An Anticholinesterase That Triggers an Excitotoxic Cascade of Oxidative Stress, Adhesion Responses, and Synaptic Compromise.European scientific journal · 2017Article
- Inhibitor of Endocannabinoid Deactivation Protects Against In Vitro and In Vivo Neurotoxic Effects of Paraoxon.Journal of molecular neuroscience : MN · 2017Article
- Inhibition of the prostaglandin E2 receptor EP2 prevents status epilepticus-induced deficits in the novel object recognition task in rats.Neuropharmacology · 2016Article
- Long-term neuropathological and behavioral impairments after exposure to nerve agents.Annals of the New York Academy of Sciences · 2016Review
- The basolateral amygdala γ-aminobutyric acidergic system in health and disease.Journal of neuroscience research · 2016Review
- A rat model of nerve agent exposure applicable to the pediatric population: The anticonvulsant efficacies of atropine and GluK1 antagonists.Toxicology and applied pharmacology · 2015Article
- Muscarinic excitation of parvalbumin-positive interneurons contributes to the severity of pilocarpine-induced seizures.Epilepsia · 2015Article
- Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Exposure to nerve agents can cause brain damage due to prolonged seizure activity, producing long-term behavioral deficits. We have previously shown that LY293558, a GluK1/AMPA receptor antagonist, is a very effective anticonvulsant and neuroprotectant against nerve agent exposure. In the present study, we examined whether the protection against nerve agent-induced seizures and neuropathology conferred by LY293558 translates into protection against pathophysiological alterations in the basolateral amygdala (BLA) and the development of anxiety, which is the most prevalent behavioral deficit resulting from exposure. LY293558 (15 mg/kg) was administered to rats, along with atropine and HI-6, at 20 min after exposure to soman (1.2 × LD50). At 24 h, 7 days, and 30 days after exposure, soman-exposed rats who did not receive LY293558 had reduced but prolonged evoked field potentials in the BLA, as well as increased paired-pulse ratio, suggesting neuronal damage and impaired synaptic inhibition; rats who received LY293558 did not differ from controls in these parameters. Long-term potentiation of synaptic transmission was impaired at 7 days after exposure in the soman-exposed rats who did not receive anticonvulsant treatment, but not in the LY293558-treated rats. Anxiety-like behavior assessed by the open field and acoustic startle response tests was increased in the soman-exposed rats at 30 and 90 days after exposure, while rats treated with LY293558 did not differ from controls. Along with our previous findings, the present data demonstrate the remarkable efficacy of LY293558 in counteracting nerve agent-induced seizures, neuropathology, pathophysiological alterations in the BLA, and anxiety-related behavioral deficits.
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