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Presence of Kynurenic Acid in the Mammalian Brain
Kynurenic acid, a tryptophan metabolite able to antagonize the actions of the excitatory amino acids, has been identified and measured for the first time in the brain of mice, rats, guinea pigs, and humans by using an HPLC method, suggesting that its turnover rate is relatively fast. Expand
Tryptophan metabolism and brain function: focus on kynurenine and other indole metabolites.
  • F. Moroni
  • Biology, Medicine
  • European journal of pharmacology
  • 30 June 1999
A number of metabolites affecting brain function originate from tryptophan metabolism and selective inhibitors of their forming enzymes may be useful to understand their role in physiology or as therapeutic agents in pathology. Expand
High mobility group box 1 protein is released by neural cells upon different stresses and worsens ischemic neurodegeneration in vitro and in vivo
Investigation of the expression levels and relocation dynamics of HMGB1 in neural cells, as well as its neuropathological potential, point to the protein as a mediator of post‐ischemic brain damage. Expand
Pharmacological characterization of 1-aminoindan-1,5-dicarboxylic acid, a potent mGluR1 antagonist.
The pharmacological profile of 1-aminoindan-1,5-dicarboxylic acid, a rigid (carboxyphenyl)glycine derivative acting on metabotropic glutamate receptors (mGluRs) is examined to suggest that AIDA is a potent, selective and competitive mGluR1 a antagonist. Expand
Pharmacological Inhibition of Histone Deacetylases by Suberoylanilide Hydroxamic Acid Specifically Alters Gene Expression and Reduces Ischemic Injury in the Mouse Brain
It is demonstrated that pharmacological inhibition ofHDACs promotes expression of neuroprotective proteins within the ischemic brain and underscores the therapeutic potential of molecules inhibiting HDACs for stroke therapy. Expand
G-protein coupled receptor 35 (GPR35) activation and inflammatory pain: Studies on the antinociceptive effects of kynurenic acid and zaprinast
It is shown that GPR35 is present in the dorsal root ganglia and in the spinal cord and the results suggest that it could be an interesting target for innovative pharmacological agents designed to reduce inflammatory pain. Expand
The Release and Neosynthesis of Glutamic Acid Are Increased in Experimental Models of Hepatic Encephalopathy
Results indicate that ammonium ions increase the release and the formation of glutamic acid in the brain and may be one of the mechanisms of ammonia toxicity in vivo. Expand
Presynaptic kynurenate‐sensitive receptors inhibit glutamate release
The data show that kynurenate‐induced inhibition of glutamate release is not mediated by glutamate receptors, and Nicotinic acetylcholine receptors may contribute to the inhibitory effects of kynurenic acid found in microdialysis studies, but not in those found in isolated synaptosomes. Expand
Kynurenine Hydroxylase Inhibitors Reduce Ischemic Brain Damage: Studies with (m-Nitrobenzoyl)-Alanine (mNBA) and 3,4-Dimethoxy-[-N-4-(Nitrophenyl)Thiazol-2YL]-Benzenesulfonamide (Ro 61-8048) in
The data suggest that inhibition of kynurenine hydroxylase could be a new avenue to reduce neuronal loss in brain ischemia. Expand