Brain-Specific Control of Kynurenic Acid Production by Depolarizing Agents

Abstract

Kynurenic acid (KYNA), a prominent tryptophan metabolite found in high concentration in urine, has recently attracted the attention of neuroscien-tists studying the function of excitatory amino acids in the brain. KYNA, which is present in the mammalian brain (Carlà et al., 1988; Turski et al., 1988; cf. Moroni et al., this volume), is a neuroinhibitory compound which exerts its effect by interacting with all three established ionotropic excitatory amino acid receptors (Foster and Fagg, 1984). In experimental systems, KYNA has also been shown to act as a neuroprotectant and anticonvulsant (Foster et al., 1984; Germano et al., 1987). Because of the inferred possible role of KYNA in human neuropsychiatrie disorders, it therefore became of interest to examine brain mechanisms which control the function of endogenous KYNA.