Homoquinolinic acid (HQA) is a potent excitotoxin[1] which is a conformationally-restricted analogue of N-methyl-D-aspartate (NMDA) and a partial agonist of the main/glutamate site of the NMDA receptor, with some selectivity for NR2B subunit-containing receptors.[2][3][4] It is approximately equipotent to NMDA and about five times more potent than quinolinic acid as an agonist of the NMDA receptor.[5] HQA has also been found to label a novel, yet uncharacterized binding site, which can be distinguished from the NMDA receptor with the use of 2-carboxy-3-carboxymethylquinoline (CCMQ), a selective ligand of the uncharacterized site.[6]

See also

References

  1. ^ Stone TW (1989). Quinolinic acid and the kynurenines. CRC Press. ISBN 978-0-8493-6592-8.
  2. ^ Stolerman IP (31 July 2010). Encyclopedia of Psychopharmacology. Springer Science & Business Media. pp. 511–. ISBN 978-3-540-68698-9.
  3. ^ de Carvalho LP, Bochet P, Rossier J (April 1996). "The endogenous agonist quinolinic acid and the non endogenous homoquinolinic acid discriminate between NMDAR2 receptor subunits". Neurochemistry International. 28 (4): 445–52. doi:10.1016/0197-0186(95)00091-7. PMID 8740453. S2CID 19395334.
  4. ^ Lemke TL, Williams DA (24 January 2012). Foye's Principles of Medicinal Chemistry. Lippincott Williams & Wilkins. pp. 404–. ISBN 978-1-60913-345-0.
  5. ^ C.S.A. Neurosciences Abstracts. Cambridge Scientific Abstracts. 1984.
  6. ^ Egebjerg J, Schousboe A, Krogsgaard-Larsen P (4 October 2001). Glutamate and GABA Receptors and Transporters: Structure, Function and Pharmacology. CRC Press. pp. 73–. ISBN 978-0-203-29938-8.