Taurine prevents ammonia-induced accumulation of cyclic GMP in rat striatum by interaction with GABAA and glycine receptors

Brain Res. 2005 May 10;1043(1-2):242-6. doi: 10.1016/j.brainres.2005.02.066.

Abstract

Previously, we had shown that ammonium chloride (ammonia)-induced accumulation of cyclic GMP in the microdialysates of rat striatum is blocked by taurine. In this study, coinfusion with taurine of a GABAA receptor antagonist bicuculline or a glycine receptor antagonist strychnine (100 microM each), separately, restored ammonia-induced release of cGMP to the extracellular fluid to approximately 29% and 18% of the level measured in the absence of taurine, respectively. Simultaneous coinfusion of both antagonists or of 100 muM picrotoxin, which is an antagonist of both GABAA and Gly receptors, offsets most of the taurine block. Ammonia-induced accumulation of cyclic GMP was attenuated by approximately 12% upon coinfusion of a GABAA receptor agonist muscimol (100 microM). The results suggest that stimulation of both GABAA and glycine receptors is involved in the mechanism by which taurine limits the activation of the NMDA/NO/cGMP pathway by ammonia in the striatum.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Ammonia / toxicity
  • Animals
  • Biomarkers
  • Corpus Striatum / drug effects*
  • Corpus Striatum / metabolism
  • Cyclic GMP / metabolism*
  • Drug Interactions
  • Male
  • Microdialysis
  • Neurotoxins / toxicity
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, GABA-A / metabolism*
  • Receptors, Glycine / metabolism*
  • Taurine / pharmacology*

Substances

  • Biomarkers
  • Neurotoxins
  • Receptors, GABA-A
  • Receptors, Glycine
  • Taurine
  • Ammonia
  • Cyclic GMP