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Quinolinic acid (QA), a tryptophan metabolite, is known to be present in many regions of the mammalian central nervous system (CNS). However, its role is still unclear. In order to evaluate the physiological role of QA in CNS, the present study was undertaken to examine its action on the spinal motoneurons of newborn rats in vitro. It wa found that QA depolarized spinal motoneurons directly. Its potency was the same as that of glutamic acid at the same concentrations. The depolarization induced by QA was strongly inhibited by 2-amino-5-phosphonovalerate (AP5), an NMDA receptor antagonist. The effect of quinolinic acid was, on the other hand, not inhibited by 6-cyano-7-nitroquinoxaline-2, 3-dione (CNQX), a non-NMDA receptor antagonist, in the presence of glycerine. These results indicate that the NMDA receptor is responsible for the QA-induced-depolarization. The possible role of QA as a transmitter is discussed.

Quinolinic acid depolarizes the spinal motoneurons of newborn rats by activating NMDA receptors.