Journal
BIOMATERIALS
Volume 34, Issue 38, Pages 10172-10181Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.biomaterials.2013.09.048
Keywords
Autophagy; LC3-I/II; QDs; Synaptic plasticity; Synapsin-I; Synapse density
Funding
- National Nature Science Foundations of China [31170965, 30970977, 31170966, 31071211, 81271492, 81371503]
- Chinese Ministry of Sciences 973 Program [2012CB932502, 2011CB504506, 2013CB933900]
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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. (C) 2013 Elsevier Ltd. All rights reserved.
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