ArticleScientific reports2019
Early Synaptic Alterations and Selective Adhesion Signaling in Hippocampal Dendritic Zones Following Organophosphate Exposure.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- Hippocampal Mitochondrial Dysfunction and Synaptic Disruption Link Organophosphate Exposure to Pre-Diabetes: An LC-MS/MS-Based Proteomics Approach.Biomolecules · 2026Article
- Ginseng extract improves synaptic resiliency: A key factor for healthy cognitive aging.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- scL-2PAM: A Novel Countermeasure That Ameliorates Neuroinflammation and Neuronal Losses in Mice Exposed to an Anticholinesterase Organophosphate.International journal of molecular sciences · 2024Article
- Mechanisms of Neurotoxicity of Organophosphate Pesticides and Their Relation to Neurological Disorders.Neuropsychiatric disease and treatment · 2024Review
- The susceptibility of humans to neurodegenerative and neurodevelopmental toxicities caused by organophosphorus pesticides.Archives of toxicology · 2023Review
- Article
- Excitotoxic stimulation activates distinct pathogenic and protective expression signatures in the hippocampus.Journal of cellular and molecular medicine · 2021Article
- Mechanisms of organophosphate neurotoxicity.Current opinion in toxicology · 2021Article
- Long pentraxin PTX3 is upregulated systemically and centrally after experimental neurotrauma, but its depletion leaves unaltered sensorimotor deficits or histopathology.Scientific reports · 2021Article
- Distinct and dementia-related synaptopathy in the hippocampus after military blast exposures.Brain pathology (Zurich, Switzerland) · 2021Article
- EGCG Promotes Neurite Outgrowth through the IntegrinEvidence-based complementary and alternative medicine : eCAM · 2021Article
- Permethrin exposure affects neurobehavior and cellular characterization in rats' brain.Environmental analysis, health and toxicology · 2020Article
- Endosomal-lysosomal dysfunction in metabolic diseases and Alzheimer's disease.International review of neurobiology · 2020Review
- The Role of Lysosomes in a Broad Disease-Modifying Approach Evaluated across Transgenic Mouse Models of Alzheimer's Disease and Parkinson's Disease and Models of Mild Cognitive Impairment.International journal of molecular sciences · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Organophosphates account for many of the world's deadliest poisons. They inhibit acetylcholinesterase causing cholinergic crises that lead to seizures and death, while survivors commonly experience long-term neurological problems. Here, we treated brain explants with the organophosphate compound paraoxon and uncovered a unique mechanism of neurotoxicity. Paraoxon-exposed hippocampal slice cultures exhibited progressive declines in synaptophysin, synapsin II, and PSD-95, whereas reduction in GluR1 was slower and NeuN and Nissl staining showed no indications of neuronal damage. The distinctive synaptotoxicity was observed in dendritic zones of CA1 and dentate gyrus. Interestingly, declines in synapsin II dendritic labeling correlated with increased staining for β1 integrin, a component of adhesion receptors that regulate synapse maintenance and plasticity. The paraoxon-induced β1 integrin response was targeted to synapses, and the two-fold increase in β1 integrin was selective as other synaptic adhesion molecules were unchanged. Additionally, β1 integrin-cofilin signaling was triggered by the exposure and correlations were found between the extent of synaptic decline and the level of β1 integrin responses. These findings identified organophosphate-mediated early and lasting synaptotoxicity which can explain delayed neurological dysfunction later in life. They also suggest that the interplay between synaptotoxic events and compensatory adhesion responses influences neuronal fate in exposed individuals.
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