Gepdiremen A, Hacimüftüoglu A, Düzenli S, Oztaş S, Süleyman H
Department of Pharmacology, Faculty of Medicine, Atatürk University, Erzurum, Turkey.
Pharmacol Res. 2000 Dec;42(6):547-51. doi: 10.1006/phrs.2000.0717.
Glutamate (10(-7)m) and one of its non-NMDA receptor agonists, kainic acid (10(-4)m), were administered to rat cerebellar granular cell cultures, and the neuroprotective role of salicylic acid was examined. Glutamate induced 38.58 +/- 1.45% neuronal cell death while kainic acid induced only 21.4 +/- 2.01% despite being 1000 times more concentrated. The most effective dose for the neuroprotective effect of salicylate in glutamate-induced neurotoxicity was 10(-5)m and it had no protective effect at 10(-7)m. With kainic acid-induced toxicity, 10(-6)m salicylate had no protective effect but 10(-5)m and. 10(-4)m salicylic acid were very effective against kainic acid-induced toxicity. As an OH-trapping agent, salicylate had a protective role in NMDA and non-NMDA receptor-activated neuronal cell death. The present study gives some important clues about oxygen free radical generation having an important role in glutamate- and kainic acid-induced neurotoxicity. On the other hand, the neuroprotective effects of salicylic acid in the present study may depend on the pH alterations in salicylic acid solutions.
