MK-801, an N-methyl-D-aspartate receptor antagonist, blocks quinolinic acid-induced lipid peroxidation in rat corpus striatum

Neurosci Lett. 1993 Sep 3;159(1-2):51-4. doi: 10.1016/0304-3940(93)90796-n.

Abstract

In this study, we evaluate the possible participation of lipid peroxidation (LP) in the neurotoxic events that follow after quinolinic acid (QUIN) microinjection into the rat corpus striatum. Two hours after QUIN (240 nmol/microliters) intrastriatal administration, lipid peroxidation was found increased by 32% vs. control as measured by thiobarbituric acid-reactive substances (TBARS). At the same time tested, the enhancement in LP was of 55% vs. control as measured by lipid fluorescent products (LFP) formation (a second index of lipid peroxidation employed). The increase of QUIN-induced lipid peroxidation was completely abolished by pretreatment of rats with an N-methyl-D-aspartate (NMDA) receptor antagonist, MK-801 (10 mg/kg, i.p.), 60 min before QUIN microinjection. Results suggest an NMDA receptor involvement in the QUIN-induced oxidative processes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Death / drug effects
  • Corpus Striatum / cytology
  • Corpus Striatum / drug effects
  • Corpus Striatum / metabolism*
  • Dizocilpine Maleate / pharmacology*
  • Lipid Peroxidation / drug effects*
  • Male
  • Neurons / drug effects
  • Quinolinic Acid / antagonists & inhibitors*
  • Quinolinic Acid / pharmacology
  • Quinolinic Acid / toxicity
  • Rats
  • Rats, Wistar
  • Receptors, N-Methyl-D-Aspartate / antagonists & inhibitors*
  • Spectrometry, Fluorescence
  • Thiobarbituric Acid Reactive Substances / metabolism

Substances

  • Receptors, N-Methyl-D-Aspartate
  • Thiobarbituric Acid Reactive Substances
  • Dizocilpine Maleate
  • Quinolinic Acid