ArticleNeurotoxicology2009
Primary brain targets of nerve agents: the role of the amygdala in comparison to the hippocampus.
Article in Neurotoxicology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
31 citing papers in PubMed, 69 citations in OpenAlex.
- Inhibiting Inducible Nitric Oxide Synthase with 1400W Reduces Soman (GD)-Induced Ferroptosis in Long-Term Epilepsy-Associated Neuropathology: Structural and Functional Magnetic Resonance Imaging Correlations with Neurobehavior and Brain Pathology.The Journal of pharmacology and experimental therapeutics · 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
- Neurological manifestations of encephalitic alphaviruses, traumatic brain injuries, and organophosphorus nerve agent exposure.Frontiers in neuroscience · 2024Review
- Article
- Characterization of Cortical Glial Scars in the Diisopropylfluorophosphate (DFP) Rat Model of Epilepsy.Frontiers in cell and developmental biology · 2022Article
- A rapidFrontiers in cellular neuroscience · 2022Article
- Assessment of four organophosphorus pesticides as inhibitors of human acetylcholinesterase and butyrylcholinesterase.Scientific reports · 2021Article
- Comparative profile of refractory status epilepticus models following exposure of cholinergic agents pilocarpine, DFP, and soman.Neuropharmacology · 2021Article
- Differential Impact of Severity and Duration ofFrontiers in cellular neuroscience · 2021Article
- Acetylcholinesterase: The "Hub" for Neurodegenerative Diseases and Chemical Weapons Convention.Biomolecules · 2020Review
- Inducible nitric oxide synthase inhibitor, 1400W, mitigates DFP-induced long-term neurotoxicity in the rat model.Neurobiology of disease · 2020Article
- In Vitro Evaluation of Neutral Aryloximes as Reactivators forBiomolecules · 2019Article
- Enaminone Modulators of Extrasynaptic αFrontiers in pharmacology · 2019Article
- The role of molecular modelling and simulation in the discovery and deployment of metal-organic frameworks for gas storage and separation.Molecular simulation · 2019Article
- Neuroprotection From Organophosphate-Induced Damage by Novel Phenoxyalkyl Pyridinium Oximes in Rat Brain.Toxicological sciences : an official journal of the Society of Toxicology · 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
- Acute and long-term consequences of exposure to organophosphate nerve agents in humans.Epilepsia · 2018Review
- Full Protection Against Soman-Induced Seizures and Brain Damage by LY293558 and Caramiphen Combination Treatment in Adult Rats.Neurotoxicity research · 2018Article
- Dexmedetomidine stops benzodiazepine-refractory nerve agent-induced status epilepticus.Epilepsy research · 2018Article
- The M1 Muscarinic Receptor Antagonist VU0255035 Delays the Development of Status Epilepticus after Organophosphate Exposure and Prevents Hyperexcitability in the Basolateral Amygdala.The Journal of pharmacology and experimental therapeutics · 2017Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Exposure to nerve agents and other organophosphorus acetylcholinesterases used in industry and agriculture can cause death, or brain damage, producing long-term cognitive and behavioral deficits. Brain damage is primarily caused by the intense seizure activity induced by these agents. Identifying the brain regions that respond most intensely to nerve agents, in terms of generating and spreading seizure activity, along with knowledge of the physiology and biochemistry of these regions, can facilitate the development of pharmacological treatments that will effectively control seizures even if administered when seizures are well underway. Here, we contrast the pathological (neuronal damage) and pathophysiological (neuronal activity) findings of responses to nerve agents in the amygdala and the hippocampus, the two brain structures that play a central role in the generation and spread of seizures. The evidence so far suggests that exposure to nerve agents causes significantly more damage in the amygdala than in the hippocampus. Furthermore, in in vitro brain slices, the amygdala generates prolonged, seizure-like neuronal discharges in response to the nerve agent soman, at a time when the hippocampus generates only interictal-like activity. In vivo experiments are now required to confirm the primary role that the amygdala seems to play in nerve agent-induced seizure generation.
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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.