Mercury modulation of GABA-activated chloride channels and non-specific cation channels in rat dorsal root ganglion neurons

Brain Res. 1991 Jun 14;551(1-2):58-63. doi: 10.1016/0006-8993(91)90913-g.

Abstract

The effects of mercuric chloride and methylmercury chloride on the rat dorsal root ganglion neurons in primary culture were studied by the whole-cell patch clamp technique. gamma-Aminobutyric acid-induced chloride currents were augmented by mercuric chloride in a potent and efficacious manner; at concentrations of 1 and 10 microM, the current amplitude was increased to 130% and 200% of the control. Methylmercury even at 100 microM did not augment but rather decreased the GABA-induced chloride current. Both mercuric chloride and methylmercury generated slow inward currents by themselves. These currents are not mediated by the GABA-activated chloride channels or by voltage-activated sodium, potassium or calcium channels, and are likely to be due to non-specific cation channels.

MeSH terms

  • Animals
  • Cations / metabolism*
  • Chloride Channels
  • Chlorides / pharmacology
  • Convulsants / pharmacology
  • Electrophysiology
  • Ganglia, Spinal / cytology
  • Ganglia, Spinal / metabolism*
  • Ganglia, Spinal / physiology
  • Ion Channels / drug effects
  • Ion Channels / metabolism*
  • Ions
  • Lanthanum / pharmacology
  • Membrane Proteins / metabolism*
  • Mercury / pharmacology*
  • Methylmercury Compounds / pharmacology
  • Neurons / metabolism
  • Neurons / physiology
  • Rats
  • Tetrodotoxin / pharmacology
  • gamma-Aminobutyric Acid / pharmacology*

Substances

  • Cations
  • Chloride Channels
  • Chlorides
  • Convulsants
  • Ion Channels
  • Ions
  • Membrane Proteins
  • Methylmercury Compounds
  • Tetrodotoxin
  • gamma-Aminobutyric Acid
  • Lanthanum
  • Mercury