Neuroprotective effect of dapsone against quinolinate- and kainate-induced striatal neurotoxicities in rats.

We tested the ability of dapsone, a well-known antibiotic and antiinflammatory drug, to attenuate both the quinolinic acid (an NMDA agonist of glutamate receptors)- and kainic acid (a non-NMDA agonist of glutamate receptors)-induced in vivo neurotoxicities in rats. Circling behaviour and striatal gamma-aminobutyric acid (GABA) depletion were considered as behavioural and neurochemical end-points of brain toxicity. Rotation behaviour, evaluated six days after the intrastriatal injection of quinolinic acid (130 +/- 19 ipsilateral turns/hr), was attenuated by doses of 12.

Systemic DL-kynurenine and probenecid pretreatment attenuates quinolinic acid-induced neurotoxicity in rats.

Kynurenine (KYN) is the precursor of kynurenic acid (KYNA), an endogenous antagonist of the glycine site of the NMDA (N-methyl-D-aspartate) receptor. Probenecid (PROB), blocks the excretion of KYNA from the extracellular fluid. KYNA antagonizes the toxic action of quinolinic acid (QUIN), an endogenous NMDA receptor agonist.