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The role of elevated autophagy on the synaptic plasticity impairment caused by CdSe/ZnS quantum dots
Link to Journal Abstract
It is well known that autophagy, a cellular stress response to degrade damaged components, can be activated by many nanoparticles. We have demonstrated that CdSe/ZnS quantum dots (QDs), which are widely applied in vitro for diagnostics and cellular imaging, can impair synaptic transmission and synaptic plasticity in the dentate gyrus (DG) area, but the mechanism is still unclear. Here we show that elevated autophagy is at least partly responsible for this synaptic dysfunction induced by QDs in vivo. QDs elicited autophagy in the HeLa cells and cultured hippocampal neurons as well, accompanied with GFP-light chain protein 3 (LC3) puncta dots and autophagosome formation, extensive conversion of LC3-I to LC3-II and a significant decrease of p62. Furthermore, we found that autophagy inhibitors (wortmannin, 3-MA or chloroquine) suppressed QDs-induced autophagic flux, partly blocked LTP impairment, coincident with down-regulation of synapsin-I and synapse deficits by QDs in the hippocampal CA1 area. Our studies have important implications in providing a potential clinical remedy for brain damage caused by nanomaterials and in designing safer nanoparticles.
In this paper, the authors show that elevated autophagy is at least partly responsible for the synaptic dysfunction induced by quantum dots (QDs) in vivo. QDs elicited autophagy in the HeLa cells and cultured hippocampal neurons as well. These studies have important implications in providing a potential clinical remedy for brain damage caused by nanomaterials and in designing safer nanoparticles.
Peer Reviewed Journal Article
Exposure Or Hazard Target
Method Of Study
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Biomaterials, 34(38): 10172-10181 (December 2013)
Chen L, Miao Y, Chen L, Jin P, Zha Y, Chai Y, Zheng F, Zhang Y, Zhou W, Zhang J, Wen L, Wang M
Last updated on January 9, 2014
This work is supported in part by the Nanoscale Science and Engineering Initiative of the National Science Foundation
under NSF Award Number EEC-0118007.
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