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ERK1/2-mediated disruption of BDNF-TrkB signaling causes synaptic impairment contributing to fluoride-induced

Jingwen Chen1, Qiang Niu1, Tao Xia1

  • 1Department of Environmental Health, MOE Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan 430030, Hubei, People's Republic of China.

Toxicology
|August 22, 2018
PubMed

Insights

Developmental fluoride exposure impairs cognitive function by disrupting synaptogenesis. This neurotoxicity involves the brain-derived neurotrophic factor (BDNF)-tyrosine kinase B (TrkB) signaling pathway, mediated by extracellular signal-regulated kinases 1 and 2 (ERK1/2).

Area of Science:

  • Neuroscience
  • Toxicology
  • Developmental Biology

Background:

  • Excessive fluoride exposure poses risks to neurodevelopment, yet underlying mechanisms are not fully understood.
  • Synaptogenesis, crucial for cognitive function, may be a target of fluoride's neurotoxic effects.

Purpose of the Study:

  • To investigate the impact of developmental fluoride exposure on synaptogenesis.
  • To elucidate the role of brain-derived neurotrophic factor (BDNF)-tyrosine kinase B (TrkB) signaling in fluoride-induced neurotoxicity.

Main Methods:

  • Utilized Sprague-Dawley rats developmentally exposed to sodium fluoride (NaF) and human neuroblastoma SH-SY5Y cells.
  • Assessed cognitive abilities, dendritic spine density, and expression of synapse proteins (SYN, PSD-95).
  • Examined the BDNF-TrkB axis and the involvement of phospho-extracellular signal-regulated kinases 1 and 2 (p-ERK1/2).

Main Results:

  • Fluoride exposure impaired cognitive function and reduced synaptic markers in rat offspring and cell models.
  • Disruption of the BDNF-TrkB signaling pathway was observed, with increased BDNF and reduced TrkB.
  • Fluoride increased p-ERK1/2 expression, and its inhibition mitigated NaF's adverse effects.

Conclusions:

  • Developmental fluoride neurotoxicity is linked to impaired synaptogenesis.
  • The ERK1/2-mediated disruption of BDNF-TrkB signaling is a key mechanism underlying fluoride's adverse effects on neurodevelopment.
Keywords:
BDNF–TrkB signalingDevelopmental neurotoxicityFluoridePhospho–ERK1/2Synaptic impairment

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