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Bisphenol A Impairs Synaptic Plasticity by Both Pre- and Postsynaptic Mechanisms.

Fan Hu1, Tingting Li1, Huarui Gong2

  • 1School of Food Science and Engineering Hefei University of Technology Hefei Anhui 230009 P. R. China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|August 31, 2017
PubMed
Summary

Juvenile exposure to Bisphenol A (BPA) impairs spatial memory and hippocampal synaptic plasticity in rats. This occurs due to reduced glutamate release, decreased dendritic spine density, and lower levels of key glutamate receptors.

Keywords:
bisphenol Ahippocampusspatial memoryspinesynaptic plasticity

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Area of Science:

  • Neuroscience
  • Environmental Health
  • Toxicology

Background:

  • Bisphenol A (BPA) is an environmental xenoestrogen linked to learning and memory deficits in rodents.
  • The precise physiological mechanisms underlying BPA's effects on synaptic plasticity remain unclear.

Purpose of the Study:

  • To investigate the impact of juvenile BPA exposure on hippocampal spatial memory and synaptic plasticity.
  • To elucidate the underlying neurobiological mechanisms, including changes in neurotransmission and receptor expression.

Main Methods:

  • Behavioral analysis of spatial memory in juvenile Sprague-Dawley rats following four weeks of BPA exposure.
  • Electrophysiological recordings to assess long-term potentiation (LTP) and presynaptic function (pulse-paired facilitation).
  • Analysis of dendritic spine density and expression of NMDA receptor 2A (NR2A) and AMPA receptor 1 (GluR1).

Main Results:

  • BPA exposure significantly impaired hippocampal spatial memory and LTP.
  • Reduced pyramidal neuron spine density, particularly on apical dendrites, was observed.
  • Presynaptic function was inhibited, suggesting decreased glutamate release.
  • Downregulation of NR2A and GluR1, and a 40% decline in NMDA-mediated excitatory postsynaptic currents (EPSCs) were noted.

Conclusions:

  • Juvenile BPA exposure negatively affects synaptic plasticity and excitatory synaptic transmission in the hippocampus.
  • These effects are attributed to decreased dendritic spine density and impaired presynaptic glutamate release.
  • The study offers insights into the long-term consequences of BPA exposure on memory throughout a rat's lifespan.