Effects of Cd(2+) on AMPA receptor-mediated synaptic transmission in rat hippocampal CA1 area

Toxicol Lett. 2008 Feb 15;176(3):215-22. doi: 10.1016/j.toxlet.2007.11.008. Epub 2007 Dec 3.

Abstract

Cadmium (Cd(2+)) is a common pollutant that causes a wide variety of toxic effects on the central nervous system. However, the mechanism of Cd(2+) neurotoxicity remains to be elucidated. In the present study, we examined the effects of Cd(2+) on AMPA receptor-mediated synaptic transmission and short-term synaptic plasticity in hippocampal CA1 area, using whole-cell patch clamp technique. Cd(2+) significantly inhibited the peak amplitude of evoked EPSCs (eEPSCs) in a concentration-dependent manner and enhanced the short-term synaptic plasticity including paired-pulse facilitation and frequency facilitation. Cd(2+) also decreased the frequency and amplitude of spontaneous EPSCs (sEPSCs) but had no effect on those of miniature EPSCs (mEPSCs). These effects of Cd(2+) may involve a presynaptic mechanism of blockade of action potential-sensitive, calcium-dependent release of glutamate. In addition, Cd(2+) prolonged the decay time of both sEPSCs and mEPSCs, which suggested a postsynaptic action site of Cd(2+). This study demonstrates that Cd(2+) impairs the Schaffer collateral-commissural-CA1 glutamatergic synaptic transmission and short-term plasticity in rat hippocampal slices, which may be a possible contributing mechanism for the Cd(2+)-induced neurotoxic effects.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cadmium Chloride / toxicity*
  • Calcium / metabolism
  • Environmental Pollutants / toxicity*
  • Excitatory Postsynaptic Potentials / drug effects*
  • Hippocampus / drug effects*
  • Hippocampus / metabolism
  • Hippocampus / physiology
  • In Vitro Techniques
  • Neuronal Plasticity / drug effects
  • Rats
  • Rats, Wistar
  • Receptors, AMPA / metabolism*
  • Time Factors

Substances

  • Environmental Pollutants
  • Receptors, AMPA
  • Cadmium Chloride
  • Calcium