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d-Glucuronolactone attenuates para-xylene-induced defects in neuronal development and plasticity in Xenopus tectum in vivo.

Authors
  • Liao, Yuan1
  • Luo, Yuhao1
  • Ding, Nanjisha1
  • Gao, Juanmei2
  • Wang, Xingbao1
  • Shen, Wanhua3
  • 1 Zhejiang Key Laboratory of Organ Development and Regeneration, College of Life and Environmental Sciences, Hangzhou Normal University, Hangzhou, Zhejiang, 310036, China. , (China)
  • 2 Zhejiang Key Laboratory of Organ Development and Regeneration, College of Life and Environmental Sciences, Hangzhou Normal University, Hangzhou, Zhejiang, 310036, China; College of Life and Sciences, Zhejiang University, Hangzhou, Zhejiang, 310036, China. , (China)
  • 3 Zhejiang Key Laboratory of Organ Development and Regeneration, College of Life and Environmental Sciences, Hangzhou Normal University, Hangzhou, Zhejiang, 310036, China. Electronic address: [email protected] , (China)
Type
Published Article
Journal
Toxicology
Publication Date
Dec 04, 2019
Volume
430
Pages
152341–152341
Identifiers
DOI: 10.1016/j.tox.2019.152341
PMID: 31811891
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Xylene and its derivatives are known to be neurotoxic to the central nervous system of animals. Our previous work has shown that para-xylene (PX) can cause an increase in apoptotic cells and abnormal avoidance behavior in Xenopus laevis. However, the mechanism underlying the impact of PX on neuronal structural and functional plasticity is less clear. Here, we examined the effects of PX on neuronal development and plasticity in the developing optic tectum. We found that HuC/D-positive neurons were more vulnerable than SOX2-positive progenitor cells or BLBP-positive radial glial cells after exposure to PX at 1 mM for 48 h. The further measurement of postsynaptic receptors and synaptic vesicle proteins showed that the expression levels of GluA1 and GluA2, but not Rab3a and SNAP25, were significantly decreased in the tectal brain. In vivo time-lapse images and electrophysiological recordings showed that PX exposure resulted in significant deficits in neuronal structure, particularly in the total dendritic branch length (TDBL), and visual stimulation-induced excitatory compound synaptic currents (eCSCs) without altering neurotransmitter release probability. Strikingly, coexposure to d-glucuronolactone (GA) and PX rescued the structural and functional deficits caused by PX exposure alone. Furthermore, we found that visual experience-induced structural, functional and behavioral plasticity was blocked by PX exposure, which was also rescued by the simultaneous administration of GA and PX . Thus, our findings indicate that PX is neurotoxic to brain development and plasticity and that GA may be considered a promising candidate to treat PX-induced defects in neural circuits. Copyright © 2019 Elsevier B.V. All rights reserved.

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