ZFIN ID: ZDB-PUB-160403-2
Microcystin-LR exposure induces developmental neurotoxicity in zebrafish embryo
Wu, Q., Yan, W., Liu, C., Li, L., Yu, L., Zhao, S., Li, G.
Date: 2016
Source: Environmental pollution (Barking, Essex : 1987)   213: 793-800 (Journal)
Registered Authors: Li, Li, Yu, Liqun
Keywords: Acetylcholine, Developmental neurotoxicity, Dopamine, MCLR, Zebrafish embryo
MeSH Terms:
  • Animals
  • Down-Regulation
  • Embryo, Nonmammalian/abnormalities
  • Embryo, Nonmammalian/drug effects*
  • Embryo, Nonmammalian/metabolism
  • Embryonic Development/drug effects*
  • Embryonic Development/genetics
  • Gene Expression/drug effects
  • Larva
  • Microcystins/toxicity*
  • Motor Activity/drug effects
  • Neurons/drug effects*
  • Neurotransmitter Agents/genetics
  • Real-Time Polymerase Chain Reaction
  • Signal Transduction
  • Up-Regulation
  • Zebrafish/abnormalities
  • Zebrafish/embryology*
  • Zebrafish/metabolism
  • Zebrafish Proteins/genetics
PubMed: 27038211 Full text @ Environ. Pollut.
Microcystin-LR (MCLR) is a commonly acting potent hepatotoxin and has been pointed out of potentially causing developmental neurotoxicity, but the exact mechanism is little known. In this study, zebrafish embryos were exposed to 0, 0.8, 1.6 or 3.2 mg/L MCLR for 120 h. MCLR exposure through submersion caused serious hatching delay and body length decrease. The content of MCLR in zebrafish larvae was analyzed and the results demonstrated that MCLR can accumulate in zebrafish larvae. The locomotor speed of zebrafish larvae was decreased. Furthermore, the dopamine and acetylcholine (ACh) content were detected to be significantly decreased in MCLR exposure groups. And the acetylcholinesterase (AChE) activity was significantly increased after exposure to 1.6 and 3.2 mg/L MCLR. The transcription pattern of manf, chrnα7 and ache gene was consistent with the change of the dopamine content, ACh content and AChE activity. Gene expression involved in the development of neurons was also measured. ɑ1-tubulin and shha gene expression were down-regulated, whereas mbp and gap43 gene expression were observed to be significantly up-regulated upon exposure to MCLR. The above results indicated that MCLR-induced developmental toxicity might attribute to the disorder of cholinergic system, dopaminergic signaling, and the development of neurons.