ArticleJournal of neurophysiology2010
Central cholinesterase inhibition enhances glutamatergic synaptic transmission.
Article in Journal of neurophysiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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.
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Who cites it
23 citing papers in PubMed, 51 citations in OpenAlex.
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- Planarian behavioral screening is a useful invertebrate model for evaluating seizurogenic chemicals.bioRxiv : the preprint server for biology · 2025Article
- Status epilepticus: Updates on mechanisms and treatments.Epilepsia open · 2025Review
- Mechanisms of Neurotoxicity of Organophosphate Pesticides and Their Relation to Neurological Disorders.Neuropsychiatric disease and treatment · 2024Review
- Biphasic response of human iPSC-derived neural network activity following exposure to a sarin-surrogate nerve agent.Frontiers in cellular neuroscience · 2024Article
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- A rapidFrontiers in cellular neuroscience · 2022Article
- Inhibition of Matrix Metalloproteinase 9 Activity Promotes Synaptogenesis in the Hippocampus.Cerebral cortex (New York, N.Y. : 1991) · 2021Article
- Persistent proteomic changes in glutamatergic and GABAergic signaling in the amygdala of adolescent rats exposed to chlorpyrifos as juveniles.Neurotoxicology · 2021Article
- Differential Impact of Severity and Duration ofFrontiers in cellular neuroscience · 2021Article
- Novel pyridinium oximes enhance 24-h survivability against a lethal dose of nerve agent surrogate in adult female rats.Toxicology · 2020Article
- Article
- Early Synaptic Alterations and Selective Adhesion Signaling in Hippocampal Dendritic Zones Following Organophosphate Exposure.Scientific reports · 2019Article
- 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
- 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
- Effects of rivastigmine and memantine alone and in combination on learning and memory in rats with scopolamine-induced amnesia.Open medicine (Warsaw, Poland) · 2015Article
- Blood glutamate scavenging as a novel neuroprotective treatment for paraoxon intoxication.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2014Article
- Somatostatin type-2 receptor activation inhibits glutamate release and prevents status epilepticus.Neurobiology of disease · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Central cholinergic overstimulation results in prolonged seizures of status epilepticus in humans and experimental animals. Cellular mechanisms of underlying seizures caused by cholinergic stimulation remain uncertain, but enhanced glutamatergic transmission is a potential mechanism. Paraoxon, an organophosphate cholinesterase inhibitor, enhanced glutamatergic transmission on hippocampal granule cells synapses by increasing the frequency and amplitude of spontaneous excitatory postsynaptic currents (sEPSCs) in a concentration-dependent fashion. The amplitude of mEPSCs was not increased, which suggested the possibility of enhanced action potential-dependent release. Analysis of EPSCs evoked by minimal stimulation revealed reduced failures and increased amplitude of evoked responses. The ratio of amplitudes of EPSCs evoked by paired stimuli was also altered. The effect of paraoxon on glutamatergic transmission was blocked by the muscarinic antagonist atropine and partially mimicked by carbachol. The nicotinic receptor antagonist α -bungarotoxin did not block the effects of paraoxon; however, nicotine enhanced glutamatergic transmission. These studies suggested that cholinergic overstimulation enhances glutamatergic transmission by enhancing neurotransmitter release from presynaptic terminals.
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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.