Heterocyclic compounds can be divided into two categories: alicyclic heterocycles and aromatic heterocycles. Compounds whose heterocycles in the molecular skeleton cannot reflect aromaticity are called alicyclic heterocyclic compounds. Compound: 492-27-3, is researched, Molecular C10H7NO3, about A Role for Xanthurenic Acid in the Control of Brain Dopaminergic Activity, the main research direction is xanthurenic acid neuroprotective agent neuropsychiatric neurodegenerative disorder; cognitive dysfunction; dopamine; kynurenic acid; schizophrenia; xanthurenic acid.SDS of cas: 492-27-3.
Xanthurenic acid (XA) is a metabolite of the kynurenine pathway (KP) synthesized in the brain from dietary or microbial tryptophan that crosses the blood-brain barrier through carrier-mediated transport. XA and kynurenic acid (KYNA) are two structurally related compounds of KP occurring at micromolar concentrations in the CNS and suspected to modulate some pathophysiol. mechanisms of neuropsychiatric and/or neurodegenerative diseases. Particularly, various data including XA cerebral distribution (from 1μM in olfactory bulbs and cerebellum to 0.1-0.4μM in A9 and A10), its release, and interactions with G protein-dependent XA-receptor, glutamate transporter and metabotropic receptors, strongly support a signaling and/or neuromodulatory role for XA. However, while the parent mol. KYNA is considered as potentially involved in neuropsychiatric disorders because of its inhibitory action on dopamine release in the striatum, the effect of XA on brain dopaminergic activity remains unknown. Here, we demonstrate that acute local/microdialysis-infusions of XA dose-dependently stimulate dopamine release in the rat prefrontal cortex (four-fold increase in the presence of 20μM XA). This stimulatory effect is blocked by XA-receptor antagonist NCS-486. Interestingly, our results show that the peripheral/i.p. administration of XA, which has been proven to enhance intra-cerebral XA concentrations (about 200% increase after 50 mg/kg XA i.p), also induces a dose-dependent increase of dopamine release in the cortex and striatum. Furthermore, our in vivo electrophysiol. studies reveal that the repeated/daily administrations of XA reduce by 43% the number of spontaneously firing dopaminergic neurons in the ventral tegmental area. In the substantia nigra, XA treatment does not change the number of firing neurons. Altogether, our results suggest that XA may contribute together with KYNA to generate a KYNA/XA ratio that may crucially determine the brain normal dopaminergic activity. Imbalance of this ratio may result in dopaminergic dysfunctions related to several brain disorders, including psychotic diseases and drug dependence.
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Reference:
Copper catalysis in organic synthesis – NCBI,
Special Issue “Fundamentals and Applications of Copper-Based Catalysts”