A glycine antagonist reduces ischemia-induced CA1 cell loss in vivo

Neurosci Lett. 1992 Sep 28;145(1):10-4. doi: 10.1016/0304-3940(92)90191-9.


Excessive activation of the N-methyl-D-aspartate (NMDA) receptor-channel complex has been implicated as one of the mechanisms by which ischemia-induced neuronal damage is mediated. Elevated glycine levels during ischemia may contribute to damage mediated by the NMDA receptor as glycine binding potentiates NMDA responses, and may be necessary for channel opening. We investigated the protective effects of 7-chlorokynurenic acid--a competitive antagonist at the glycine binding site associated with the NMDA receptor--against hippocampal CA1 cell loss induced by transient forebrain ischemia in rats. Intraventricular administration of the drug immediately before the onset of ischemia significantly attenuated neuronal loss compared to vehicle-treated animals.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Glycine / antagonists & inhibitors*
  • Hippocampus / pathology*
  • Injections, Intraventricular
  • Ischemic Attack, Transient / drug therapy*
  • Ischemic Attack, Transient / pathology
  • Kynurenic Acid / analogs & derivatives*
  • Kynurenic Acid / pharmacology
  • Male
  • Pyramidal Tracts / pathology
  • Rats
  • Rats, Wistar
  • Receptors, Glycine
  • Receptors, N-Methyl-D-Aspartate / antagonists & inhibitors*
  • Receptors, N-Methyl-D-Aspartate / drug effects
  • Receptors, Neurotransmitter / antagonists & inhibitors
  • Seizures / physiopathology


  • Receptors, Glycine
  • Receptors, N-Methyl-D-Aspartate
  • Receptors, Neurotransmitter
  • Kynurenic Acid
  • 7-chlorokynurenic acid
  • Glycine