Cited by 68Genetic Neurodegenerative DiseasesNeuroscience and Neuropharmacology ResearchNitric Oxide and Endothelin Effects

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Nitric Oxide Synthase Inhibition Prevents Acute Quinolinate-Induced Striatal Neurotoxicity

Pérez-Severiano, Francisca, Escalante, Bruno, Ríos, Camilo·1998·Neurochemical Research

Abstract

Quinolinic acid (QUIN) is an endogenous excitotoxin acting on N-methyl-D-aspartate (NMDA) receptors, that leads to neurotoxic damage resembling the alterations observed in Huntington's disease. Two major end-points of QUIN induced neurotoxicity are both circling behavior (CB) and lipid peroxidation (LP). Recently, nitric oxide (NO) has been implicated as a mediator of cell injury in some neurological disorders, thus, NO as a free radical might be involved in QUIN-induced neurotoxicity and oxidative stress. In the present study we evaluated the possible role of NO on QUIN-induced neurotoxicity, by measuring nitric oxide synthase activity (NOS), before and after QUIN-induced damage and by evaluating the effect of NOS inhibition on acute QUIN-induced CB and LP. Rats were striatally microinjected with QUIN (240 nmol/microl). QUIN administration increased NOS activity by 327% as compared to control values and this enhancement was inhibited by i.v. pretreatment with a NOS inhibitor the N(G)-nitro-L-arginine methyl ester (L-NAME) (10 mg/kg). QUIN-induced CB was also attenuated by pretreatment of rats with 1, 5, 10 and 15 mg/kg of L-NAME by -37, -55, -62 and -74% vs QUIN respectively. Similarly, L-NAME also reduced by 32% the QUIN-induced LP. These findings suggest that enhanced NOS activity may participate in QUIN-induced neurotoxicity and oxidative stress.

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  1. Perkins, M. N., and Stone, T. W. 1983. Pharmacology and regional variations of quinolinic acid evoked excitations in the rat central nervous system. J. Pharmacol. Exp. Ther. 226:551-557. · DOI
  2. Schwarcz, R., Whetsell, W. O., and Mangano, R. M. 1983. Quinolinic acid: an endogenous metabolite that produces axon-sparing lesions in rat brain. Science. 219:316-318. · DOI
  3. Beal, M. F., Kowall, N. W., Ellison, D. W., Mazurek, M. F., Schwarcz, K. J., and Martin, J. B. 1986. Replication of the neurochemical characteristics of Huntington's disease by quinolinic acid. Nature. 321:168-171. · DOI
  4. Reynolds, G. P., Pearson, S. J., Halket, J., and Sandler, M. 1988. Brain quinolinic acid in Huntington's disease. J. Neurochem. 50:1959-1960. · DOI
  5. Stone, T. W. 1993. Neuropharmacology of quinolinic and kynurenic acids. Pharmacol. Rev. 45(3):309-379. · DOI
  6. Wolfensberger, M., Amsler, U., Cuenod, M., Foster, A. C., Whetsell, W. O., and Schwarcz, R. 1983. Identification of quinolinic acid in rat and human brain tissue. Neurosci. Lett. 41:247-252. · DOI
  7. Moroni, F., Lombardi, G., Moneti, G., and Aldino, G. 1984. The excitotoxin quinolinic acid is present in the brain of several mammals and it's cortical contents increases during the aging process. Neurosci. Lett. 47:51-55. · DOI
  8. Beal, M. F., Matson, W. R., Swartz, K. J., Gamache, P. H., and Bird, E. D. 1990. Kynurenine pathway measurements in Huntington's disease striatum: Evidence for reduced formation of kynurenic acid. J. Neurochem. 55:1327-1339. · DOI
  9. Albin, R. L., Young, A. B., Penney, J. B., Handelin, B., Balfour, R., et al. 1990. Abnormalities of striatal projection neurons and N-methyl-D-aspartate receptors in presymptomatic Huntington's diseases. N. Engl. J. Med. 322:1293-1298. · DOI
  10. Heyes, M. P., Saito, K., Crowlwy, J. S., Davis, L. E., Demitrack, M. A., et al. 1992. Quinolinic acid and kynurenine pathway metabolism in inflammatory and non-inflammatory disease. Brain. 115:1249-1273. · DOI
  11. Ríos, C., and Santamaría, A. 1991. Quinolinic acid is a potent lipid peroxidant in rat brain homogenates. Neurochem. Res. 16(10):1139-1143. · DOI
  12. Santamaría, A., and Ríos, C. 1993. MK-801, an N-methyl-D-aspartate receptor antagonist, blocks quinolinic acid-induced lipid peroxidation in rat corpus striatum. Neurosci. Lett. 159:51-54. · DOI
  13. Susel, Z., Engber, T. M., and Chase, T. N. 1989. Behavioral evaluation of the anti-excitotoxic properties of MK-801: comparison with neurochemical measurements. Neurosci. Lett. 104:125-129. · DOI
  14. Schmidt, W., Wolf, G., Calka, J., and Schmidt, H. H. H. W. 1995. Evidence for bidirectional changes in nitric oxide synthase activity in the rat striatum after excitotoxically (quinolinic acid) induced degeneration. Neuroscience. 67(2):345-356. · DOI
  15. Moncada, S., Palmer, R. M. J., and Higgs, E. A. 1991. Nitric oxide: physiology, pathophysiology and pharmacology. Pharmacol. Rev. 43:109-143. · DOI · Paper page
  16. Chapman, P. F., Atkins, C. M., Allen, M. T., et al. 1992. Inhibition of nitric oxide synthesis impairs two different forms of learning. NeuroReport. 3:567-570. · DOI
  17. O'Dell, T. J., Hawkins, R. D., Kandel, E. R., and Arancio, O. 1991. Test of the roles of two diffusable substances in long term potentiation: Evidence for nitric oxide as a possible early retrograde messenger. Proc. Natl. Acad. Sci. U.S.A. 88:1185-1289. · DOI
  18. Rubbo, H., Radi, R., Trujillo, M., Telleri, R., Kalyanaraman, B., et. al. 1994. Nitric oxide regulation of superoxide and peroxinitrite-depend lipid peroxidation. J. Biol. Chem. 269(42):26066-26091. · DOI
  19. Lipton, S. A., and Stamler, J. S. 1994. Actions of redox congeners of nitric oxide at the NMDA receptor. Neuropharmacol. 33(11):1229-1233. · DOI
  20. Garthwaite, G., and Garthwite, J. 1988. Cyclic GMP and cell death in rat cerebelar slices. Neuroscience. 26:321-326. · DOI
  21. Dawson, V. L., Dawson, T. M., London, E. D., Bredt, D. S., and Snyder, S. H. 1991. Nitric oxide mediates glutamate neurotoxicity in primary cortical cultures. Proc. Natl. Acad. Sci. USA. 88:6368-6371. · DOI · Paper page
  22. Garthwaite, J. 1991. Glutamate, nitric oxide and cell-cell signaling in the neurons system. Trend Neurosci. 14:60-67. · DOI
  23. Kiedrowski, L., Costa, E., Wroblewski, J. T. 1992. In vitro interaction between cerebelar astrocytes and granule cells: a putative role for nitric oxide. Neurosci. Lett. 135:59-61. · DOI
  24. Paxinos, G., and Watson, G. 1984. The rat brain in stereotaxic coordinates, Sydney, Academic Press.
  25. Giordano, M., Ford, L. M., Braucman, J. L., Norman, A. B., and Sanberg, P. R. 1990. MK-801 Prevents quinolinic acid-induced behavioral deficits and neurotoxicity in the striatum. Brain Res. Bull. 24:313-319. · DOI
  26. Moore, P. K., Al-Swayeh, O. A., Chong, N. W. S., Evans, R. A., and Gibson, A. 1990. L-NG-nitro-arginine (L-NOARG), a novel, L-arginine-reversible inhibitor of endothelium-dependent vasodilatation in vitro. Br. J. Pharmacol. 99:408-412. · DOI
  27. Bredt, D. S., and Snyder, S. H. 1990. Isolation of nitric oxide synthase, a calmodulin-requiring enzyme. Proc. Natl. Acad. Sci. USA. 87:682-685. · DOI
  28. Bradford, M. M. 1976. A rapid and sensitive method for the quantification of protein dye binding. Anal. Biochem. 72:248-254. · DOI · Paper page
  29. Triggs, W. P., and Willmore, L. J. 1984. In vivo lipid peroxidation in rat brain following intracortical Fe++ injection. J. Neurochem. 42:976-979. · DOI
  30. Lowry, O. H., Rosebrough, N. J., Farr, A. L., and Randall, R. J. 1951. Protein measurement with the folin-phenol reagent. J. Biol. Chem. 193:265-275. · DOI
  31. Schwarcz, R., Fuxe, K., Agnati, L. F., Hockfelt, T., and Coyle, J. T. 1979. Rotational behavior in rats with unilateral striatal kainic lesions: a behavioral model for studies on intact dopamine receptors. Brain Res. 170:485-495. · DOI
  32. Fisher, R. S. 1991. Introduction to the excitatory amino acid system. Epilepsy. 10:3-8.
  33. Fisher, R. S. 1991. Glutamate and epilepsy. Neurotransmitters Epilepsy. 11:131-45.
  34. Turski, L., Bressler, K., Rettig, K. J., Loschmann, P. A., and Wachtel, H. 1991. Protection of substantia nigra from MPTP+ neurotoxicity by N-methyl-D-aspartate antagonists. Nature. 349:414-18. · DOI
  35. Lipton, S. A., Sucher, N. J., Kaiser, P. K., and Dreyer, E. B. 1991. Synergistic effects of HIV coat protein and NMDA receptor-mediated neurotoxicity. Neuron. 7:111-18. · DOI
  36. Jansen, K. L. R., Faull, R. L. M., Dragunow, M., and Synek, B. L. 1990. Alzheimer's disease-changes in hippocampal N-methyl-D-aspartate, quisqualate, neurotensin, adenosine, benzodiazepine, serotonin and apioid receptors an autoradiographic study. Neurosci. 39:613-27. · DOI
  37. Choi, D. W. 1988. Glutamate neurotoxicity and diseases of the nervous system. Neuron. 1:623-34. · DOI
  38. Simonian, N. A., and Coyle, J. T. 1996. Oxidative stress in neurodegenerative diseases. Annu. Rev. Pharmacol. Toxicol. 36:83-106. · DOI · Paper page
  39. Heyes, M. P., Brew, B. J., Martin, A., Price, R. W., and Salazar A. M. 1991. Quinolinic acid in cerebrospinal fluid and serum in HIV-1 infection: relationship to clinical and neurologic status. Ann. Neurol. 29:202-209. · DOI
  40. Heyes, M. P. 1996. The kinurenine pathway and neurologic disease. Therapeutic strategies. Adv. Exp. Med. Biol. 398:125-9. · DOI
  41. Strijbos, P. J., Leach, M. J., and Garthwaite, J. 1996. Vicious cycle involving Na+ channels, glutamate release and NMDA receptors mediates delayed neurodegeneration through nitric oxide formation. Neurosci. Res. 16(16):5004-13.
  42. Park, S. K., Grzybicki D., Lin, H. L., and Murphy, S. 1994. Modulation of inducible nitric oxide synthase expression in astroglial cells. Neuropharmacol. 33(11):1419-1423. · DOI
  43. Moncada, S., Herman, A. G., and Vanhoutte, P. M. 1987. Endothelium-derived relaxing factor is identified as nitric oxide. Trends Pharmacol. Sci. 8:365-367. · DOI
  44. Galasso, J. M., Bazzett, T. J., Becker, J. B., and Albin, R. L. 1995. Synergistic effect of intraestriatal coadministration of L-NAME and quinolinic acid. Neuro Report. 6:1505-1608.
  45. Globus, M. Y.-T., Prado, R., Sanchez-Ramos, J., Zhao, Weizhao., Dietrich, W. D., Busto, R., and Ginsberg, M. D. 1995. A dual Role for nitric oxide in NMDA-mediated toxicity in vivo. J. Cerebral Blood Flow and Metabolism. 15:904-913. · DOI
  46. Lancelot, E., Callebert, J., Lerouet, D., Revaud, M. L., Boulou, R. G., Plotkine, M. (1995): Role of the L-arginine-nitric oxide pathway in the basal hydroxyl radical production in the striatum of awake rats as measured by brain microdialisis. Neuroscience Letters. 202:21-24. · DOI

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Metadata

Authors
Pérez-Severiano, F., Escalante, B., & Ríos, C.
Affiliations
Instituto Politécnico Nacional (MX)
Venue
Neurochemical Research
Published
1998-10
Volume
23
Issue
10
Pages
1297-1302
ISSN
  • 0364-3190 (ISSN-L)
  • 1573-6903
OpenAlex
W2113919453
Cited by
68
References
0
Citations by year
2024: 1 · 2022: 1 · 2021: 1 · 2020: 1 · 2018: 2 · 2017: 3 · 2016: 2 · 2015: 4 · 2013: 3
FWCI
1.71
Type
journal article
Language
en
Open access
closed
Locations
  • Neurochemical Research (publishedVersion)
  • PubMed (publishedVersion)
Funders
Consejo Nacional de Ciencia y Tecnología
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Genetic Neurodegenerative Diseases
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Keywords
quinolinic acid, nitric oxide synthase, striatal neurotoxicity, NMDA receptor excitotoxicity, circling behavior, lipid peroxidation, oxidative stress, L-NAME, Huntington's disease model
MeSH terms
Animals, Corpus Striatum, Enzyme Inhibitors, Male, Motor Activity, Rats, Wistar, Quinolinic Acid, Nitric Oxide Synthase, NG-Nitroarginine Methyl Ester, Rats

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CoChat. (2026). Citation check: Nitric Oxide Synthase Inhibition Prevents Acute Quinolinate-Induced Striatal Neurotoxicity. https://app.cochat.ai/papers/10.1023/a:1020700401678
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Pérez-Severiano, F., Escalante, B., & Ríos, C. (1998). Nitric Oxide Synthase Inhibition Prevents Acute Quinolinate-Induced Striatal Neurotoxicity. Neurochemical Research. https://doi.org/10.1023/a%3A1020700401678