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Direct Quantification of Nanoplastics Neurotoxicity by Single‐Vesicle Electrochemistry
Summary
Using single-vesicle electrochemistry, this study provides the first direct measurement of how nanoplastics disrupt neurotransmitter release at the level of individual nerve cells. Polystyrene nanoplastics taken up by neurons disrupted the cellular machinery controlling how vesicles fuse and release catecholamines (like dopamine and norepinephrine), reducing both the amount of neurotransmitter released and the frequency of release events. These findings are concerning because they suggest nanoplastic exposure could interfere with normal brain signaling at concentrations that don't immediately kill cells.
Abstract 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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