Overview
- Traynelis, S.F. et al. (2010) Pharmacol. Rev. 62, 405.
- Birch, P.J. et al. (1988) Eur. J. Pharmacol. 154, 85.
Alomone Labs Kynurenic acid inhibits NMDA (NR1+NR2A) channels expressed in Xenopus oocytes.A. Time course of NMDA currents elicited by stimulation with 100 µM glutamate and 100 µM glycine, every 50 sec, while membrane potential was held at -80 mV. 100 and 250 µM Kynurenic acid (#K-110), applied for 3 min each, reversibly inhibited current amplitude. B. Superimposed current traces taken from the experiment described in A.
Kynurenic acid (KYNA) is a neuroactive metabolite of the kynurenine pathway of tryptophan degradation. It is a competitive and broad spectrum antagonist of glutamate receptors. Additionally, KYNA antagonizes α7 nicotinic acetylcholine receptor and G-protein coupled GPR35 receptor. KYNA is widely used as a pharmacological tool to experimentally eliminate activation of all these receptors in vivo or in vitro1-3.
Kynurenine can influence brain function and its levels in the human brain are significantly higher compared to those in other species. Its levels in the brain are normally determined by local neosynthesis from its bioprecursor kynurenine pathway metabolite, since KYNA is not actively transported through the blood-brain barrier.
KYNA serves as a substrate for the probenecid-sensitive organic anion transporters OAT1 and OAT3. These proteins are present in brain capillary endothelial cells, thus it is likely that these proteins play an important role in the elimination of KYNA from the brain’s extracellular compartment2.
KYNA has antioxidant properties and has the ability to eliminate hydroxyl, superoxide anion and other free radicals3.
It has been documented that in animal models KYNA may have a positive influence on the number of pathologies in the gastrointestinal tract such as ulcers, colon obstruction and colitis1.
