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Direct Quantification of Nanoplastics Neurotoxicity by Single‐Vesicle Electrochemistry
Summary
Using a precise electrochemical technique to measure individual brain cell vesicles, researchers provided the first direct evidence that nanoplastics disrupt how neurons store and release chemical messengers. Nanoplastic exposure reduced the amount of neurotransmitters in cell vesicles and impaired the process of releasing them during signaling. The study offers a detailed molecular-level look at how nanoplastics may interfere with brain cell communication.
Nanoplastics are recently recognized as neurotoxic factors for the nervous systems. However, whether and how they affect vesicle chemistry (i.e., vesicular catecholamine content and exocytosis) remains unclear. This study offers the first direct evidence for the nanoplastics-induced neurotoxicity by single-vesicle electrochemistry. We observe the cellular uptake of polystyrene (PS) nanoplastics into model neuronal cells and mouse primary neurons, leading to cell viability loss depending on nanoplastics exposure time and concentration. By using single-vesicle electrochemistry, we find the reductions in the vesicular catecholamine content, the frequency of stimulated exocytotic spikes, the neurotransmitter release amount of single exocytotic event, and the membrane-vesicle fusion pore opening-closing speed. Mechanistic investigations suggest that PS nanoplastics can cause disruption of filamentous actin (F-actin) assemblies at cytomembrane zones and change the kinetic patterns of vesicle exocytosis. Our finding shapes the first quantitative picture of neurotoxicity induced by high-concentration nanoplastics exposure at a single-cell level.
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