ZFIN ID: ZDB-PUB-190512-11
Silver nanoparticles induce abnormal touch responses by damaging neural circuits in zebrafish embryos
Zhao, G., Wang, Z., Xu, L., Xia, C.X., Liu, J.X.
Date: 2019
Source: Chemosphere   229: 169-180 (Journal)
Registered Authors: Liu, Jing-xia
Keywords: AgNPs, Electrical membrane properties, Neural circuits, Touch responses
MeSH Terms:
  • Animals
  • Embryo, Nonmammalian/drug effects*
  • Embryo, Nonmammalian/physiology
  • Metal Nanoparticles/toxicity*
  • Nervous System Physiological Phenomena/drug effects*
  • Silver/chemistry*
  • Silver/toxicity*
  • Touch/drug effects*
  • Touch/physiology
  • Zebrafish/embryology*
  • Zebrafish/metabolism
  • Zebrafish/physiology
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed: 31078031 Full text @ Chemosphere
ABSTRACT
Although silver nanoparticles (AgNPs) are used in various commercial products, the biological effects of AgNPs on fish embryogenesis and the underlying molecular mechanisms are still poorly understood. In this study, both touch responses and neuron membrane potential were found to be abnormal in AgNPs-stressed embryos. Moreover, neurogenesis genes were unveiled to be down-regulated and were enriched in ligand-gated ion channel activity, dopamine receptor signaling pathway, etc. in AgNPs-stressed embryos by microarray assays. Additionally, the down-regulated expression of otpa/sncgb - gad1b/gad2 dopaminergic neurotransmitter genes, robo2 - vim and glrbb synaptic transmission genes, and motor neuron genes isl1 &isl2a was further identified in both AgNPs- and Ag+-stressed embryos by qPCR, whole-mount in situ hybridization (WISH), and by using specific promoter-derived GFP fluorescence transgenic zebrafish. Moreover, the reduced expression of gad1b, gad2, and isl1 could be recovered by adding Ag+ chelating compound l-cysteine in AgNPs stressed embryos. Our results reveal for the first time that it is through damaging the formation of neural circuits, including dopaminergic neurotransmitter, synaptic transmission, and motor activities, that AgNPs induce abnormal electrical membrane properties, leading to dysfunctional touch responses and locomotor escape responses mostly via their released Ag+ during embryogenesis.
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