Backgrounds: Quinolinic acid (QUIN) is an endogenous metabolite of L-tryptophan produced by kynurenine pathway. Elevated levels have been reported in (neuro)inflammatory diseases of the central nervous system and also in the gastrointestinal tract. Kynurenic acid, another metabolite of the kynurenine pathway, an antagonist of NMDA receptors is neuroprotective, and recent work revealed a modulatory effect on colonic motility in an experimental model of colitis. QUIN is an agonist at glutamate receptors and at high concentrations or after long exposure in moderate concentrations a neuronal excitotoxic effect has been demonstrated in the central nervous system. Similar neurotoxic effect of QUIN on the enteric neurons, and the possible role of QUIN in changes of gastrointestinal motility have not been investigated. The aim of this study was to investigate the acute and chronic effect of QUIN on gastrointestinal motility. Materials and methods: Adult CFLP male mice weighing 30g were used for the experiments. The total gastrointestinal transit (WGT), the small intestinal transit (SIT) were tested by the administration test meal containing carmine red is not absorbed in the gastrointestinal tract. The distal colonic transit (DCT) was tested by bead expulsion test. As an acute challenge mice received a single dose of 100mg/kgbwt QUIN intraperitoneally, and this dose was administered daily for 35 days in the chronic experiments. Bodyweights were also recorded during the chronic experiments. Results: Acute QUIN challenge caused a significant delay in WGT (306min in 14 treated vs. 215min in 12 control mice; p<0.01) but did not affect significantly the SIT and DCT. The chronic QUIN treatment significantly accelerated the WGT (median: 187min in the 13 treated vs. 287min in the 11 control mice; p<0.02) without having a significant effect either on SIT or on DCT. There was no difference between the bodyweight gains of the chronic QUIN treated and control groups of mice. Conclusion: Both acute and chronic QUIN administration influences gastrointestinal motility in mice. The underlying mechanisms and their role in pathological conditions warrant further studies.