Cited by 30Parkinson's Disease Mechanisms and TreatmentsNuclear Receptors and SignalingNeuroprotection in Cerebral Ischemia

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The role of nitric oxide on visual-evoked potentials in MPTP-induced Parkinsonism in mice

Aras, Sinem, Tanriover, Gamze, Aslan, Mutay, Yargicoglu, Piraye, Agar, Aysel·2014·Neurochemistry International

Abstract

The present study aimed to elucidate visual evoked potentials (VEP) changes in MPTP induced Parkinson's disease (PD) and investigate the possible benefical effects of neuronal (n) and inducible (i) nitric oxide synthase (NOS) inhibitors on altered VEPs, lipid peroxidation and apoptosis. 3 months old C57BL/6 mice were randomly divided into 6 groups which included control (C), 7-nitra indazole treated (7-NI), S-methylisothiourea (SMT) treated, 1,2,3,6-tetrahydropyridine (MPTP) treated, 7-NI+MPTP treated and SMT+MPTP treated. Motor activity of mice was evaluated via the pole test. At the end of the experimental period VEPs were recorded, brain and retina tissues were removed for biochemical analysis. Dopaminergic neuron death at substantia nigra (SN) was determined by immunohistochemical analysis of tyrosine hydroxylase (TH). Immunohistochemical staining was also performed to determine iNOS and nNOS in all tissue sections. Mice with experimental PD exhibited decreased motor activity. Dopaminergic cell death at pars compacta of SN (SNpc) was significantly increased in MPTP treated group compared to control. Diminished Parkinsonism symptoms were observed in 7-NI+MPTP and SMT+MPTP groups. Treatment with 7-NI and SMT decreased dopaminergic cell death in MPTP treated mice. Caspase-3 activity, nitrite/nitrate and 4-hydroxynonenal (4-HNE) levels were significantly increased in SN of MPTP treated mice compared to control. Treatment with 7-NI and SMT significantly decreased elevated caspase-3 activity, nitrite/nitrate and 4-HNE levels in SN of MPTP treated mice. No significant difference in above parameters were observed in the retina. VEP latencies were significantly prolonged in MPTP group compared to control group. 7-NI and SMT treatment caused a significant decrease in VEP latencies in MPTP treated mice compared to none treated MPTP group. This data shows that 7-NI and SMT improves prolonged VEP latencies. The protective effects of 7-NI and SMT on VEP alterations can be related to decreased dopaminergic cell death and reduced lipid peroxidation.

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Research works printed but not linked: 55

  1. Baltazar, 2014, Pesticides exposure as etiological factors of Parkinson’s disease and other neurodegenerative diseases-a mechanistic approach, Toxicol. Lett., 10.1016/j.toxlet.2014.01.039 · DOI
  2. Baraboi, 1989, The role of lipid peroxidation in the mechanism of stress, Fiziol. Zh., 35, 85
  3. Bazzu, 2010, Alpha-Synuclein- and MPTP-generated rodent models of Parkinson’s disease and the study of extracellular striatal dopamine dynamics: a microdialysis approach, CNS Neurol. Disord. Drug Targets., 9, 482, 10.2174/187152710791556177 · DOI
  4. Betarbet, 2002, Animal models of Parkinson’s disease, BioEssays, 24, 308, 10.1002/bies.10067 · DOI
  5. Bodis-Wollner, 1978, Measurements of visual evoked potentials in Parkinson’s disease, Brain, 101, 661, 10.1093/brain/101.4.661 · DOI
  6. Boo, 2007, An improved method to measure nitrate/nitrite with an NO-selective electrochemical sensor, Nitric Oxide, 16, 306, 10.1016/j.niox.2006.09.004 · DOI
  7. Brown, 2010, Nitric oxide and neuronal death, Nitric Oxide, 23, 153, 10.1016/j.niox.2010.06.001 · DOI
  8. Brzozowski, 2011, The effect of nNOS inhibitors on toxin-induced cell death in dopaminergic cell lines depends on the extent of enzyme expression, Brain Res., 1404, 21, 10.1016/j.brainres.2011.05.063 · DOI
  9. Bugnon, 1994, Nitric oxide modulates endogenous dopamine release in bovine retina, Neuroreport, 5, 401, 10.1097/00001756-199401120-00007 · DOI
  10. Buttner, 1996, Chromatic and achromatic visual evoked potentials in Parkinson’s disease, Electroencephalogr. Clin. Neurophysiol., 100, 443, 10.1016/0168-5597(96)95700-7 · DOI
  11. Castagnoli, 2001, Neuroprotection in the MPTP Parkinsonian C57BL/6 mouse model by a compound isolated from tobacco, Chem. Res. Toxicol., 14, 523, 10.1021/tx000224v · DOI
  12. Celesia, 1984, Evoked potential techniques in the evaluation of visual function, J. Clin. Neurophysiol., 1, 55, 10.1097/00004691-198401000-00003 · DOI
  13. Date, 1990, Long-term effect of MPTP in the mouse brain in relation to aging: neurochemical and immunocytochemical analysis, Brain Res., 519, 266, 10.1016/0006-8993(90)90088-S · DOI
  14. Di Matteo, 2009, Involvement of nitric oxide in nigrostriatal dopaminergic system degeneration: a neurochemical study, Ann. N. Y. Acad. Sci., 1155, 309, 10.1111/j.1749-6632.2008.03678.x · DOI
  15. Djamgoz, 1995, Nitric oxide inhibits depolarization-induced release of endogenous dopamine in the rabbit retina, Neurosci. Lett., 198, 33, 10.1016/0304-3940(95)11958-Y · DOI
  16. Du, 2001, Minocycline prevents nigrostriatal dopaminergic neurodegeneration in the MPTP model of Parkinson’s disease, Proc. Natl. Acad. Sci. U.S.A., 98, 14669, 10.1073/pnas.251341998 · DOI · Paper page
  17. Eberhardt, 2003, Apoptotic mechanisms and antiapoptotic therapy in the MPTP model of Parkinson’s disease, Toxicol. Lett., 139, 135, 10.1016/S0378-4274(02)00428-9 · DOI
  18. Guo, 2007, Protective effects of green tea polyphenols in the 6-OHDA rat model of Parkinson’s disease through inhibition of ROS-NO pathway, Biol. Psychiatry, 62, 1353, 10.1016/j.biopsych.2007.04.020 · DOI
  19. Gutteridge, 1994, Biological origin of free radicals, and mechanisms of antioxidant protection, Chem. Biol. Interact., 91, 133, 10.1016/0009-2797(94)90033-7 · DOI
  20. Hattoria, 2009, Toxic effects of dopamine metabolism in Parkinson’s disease, Parkinsonism Relat. Disord., 15
  21. Hesslinger, 2009, Inhibition of inducible nitric oxide synthase in respiratory diseases, Biochem. Soc. Trans., 37, 886, 10.1042/BST0370886 · DOI
  22. Iravani, 2002, Involvement of inducible nitric oxide synthase in inflammation-induced dopaminergic neurodegeneration, Neuroscience, 110, 49, 10.1016/S0306-4522(01)00562-0 · DOI · Paper page
  23. Jenner, 1998, Oxidative mechanisms in nigral cell death in Parkinson’s disease, Mov. Disord., 13, 24
  24. Ji, 2001, 4-Hydroxynonenal induces apoptosis via caspase-3 activation and cytochrome c release, Chem. Res. Toxicol., 14, 1090, 10.1021/tx000186f · DOI
  25. Kalgutkar, 1992, Synthesis of novel MPTP analogs as potential monoamine oxidase B (MAO-B) inhibitors, J. Med. Chem., 35, 4165, 10.1021/jm00100a023 · DOI
  26. Kastner, 1994, Decreased tyrosine hydroxylase content in the dopaminergic neurons of MPTP-intoxicated monkeys: effect of levodopa and GM1 ganglioside therapy, Ann. Neurol., 36, 206, 10.1002/ana.410360213 · DOI
  27. Kidd, 2000, Parkinson’s disease as multifactorial oxidative neurodegeneration: implications for integrative management, Altern. Med. Rev., 5, 502
  28. Kishimoto, 1996, Immobilization-induced stress activates neuronal nitric oxide synthase (nNOS) mRNA and protein in hypothalamic–pituitary–adrenal axis in rats, Brain Res., 720, 159, 10.1016/0006-8993(96)00101-1 · DOI
  29. Krukoff, 1999, Central actions of nitric oxide in regulation of autonomic functions, Brain Res. Brain Res. Rev., 30, 52, 10.1016/S0165-0173(99)00010-7 · DOI
  30. Kucukatay, 2006, Visual evoked potentials in normal and sulfite oxidase deficient rats exposed to ingested sulfite, Neurotoxicology, 27, 93, 10.1016/j.neuro.2005.07.002 · DOI
  31. Langheinrich, 2000, Visual contrast response functions in Parkinson’s disease: evidence from electroretinograms, visually evoked potentials and psychophysics, Clin. Neurophysiol., 111, 66, 10.1016/S1388-2457(99)00223-0 · DOI
  32. Levecque, 2003, Association between Parkinson’s disease and polymorphisms in the nNOS and iNOS genes in a community-based case-control study, Hum. Mol. Genet., 12, 79, 10.1093/hmg/ddg009 · DOI
  33. Lima, 2014, Nitric oxide as a regulatory molecule in the processing of the visual stimulus, Nitric Oxide, 36, 44, 10.1016/j.niox.2013.10.011 · DOI
  34. Neal, 1999, Release of endogenous ascorbic acid preserves extracellular dopamine in the mammalian retina, Invest. Ophthalmol. Vis. Sci., 40, 2983
  35. Nightingale, 1986, Visual evoked cortical potentials and pattern electroretinograms in Parkinson’s disease and control subjects, J. Neurol. Neurosurg. Psychiatry, 49, 1280, 10.1136/jnnp.49.11.1280 · DOI
  36. O’Donnell, 1997, Nitric oxide inhibition of lipid peroxidation: kinetics of reaction with lipid peroxyl radicals and comparison with alpha-tocopherol, Biochemistry, 36, 15216, 10.1021/bi971891z · DOI
  37. Ogawa, 1997, Dopamine neurotransmission and treatments for Parkinson’s disease in the molecular biology era, Eur. Neurol., 38, 2, 10.1159/000113435 · DOI
  38. Okuda, 1995, Visual evoked potentials (VEPs) in Parkinson’s disease: correlation of pattern VEPs abnormality with dementia, Alzheimer Dis. Assoc. Disord., 9, 68, 10.1097/00002093-199509020-00002 · DOI
  39. O’Mahony, 1993, Parkinson’s dementia and Alzheimer’s dementia: an evoked potential comparison, Gerontology, 39, 228, 10.1159/000213538 · DOI
  40. Ozsoy, 2011, The effect of docosahexaenoic acid on visual evoked potentials in a mouse model of Parkinson’s disease: the role of cyclooxygenase-2 and nuclear factor kappa-B, Neurotox. Res., 20, 250, 10.1007/s12640-011-9238-y · DOI
  41. Pall, 1986, Lipid peroxidation and Parkinson’s disease, Lancet, 2, 870, 10.1016/S0140-6736(86)92913-2 · DOI
  42. Pang, 2010, Light responses and morphology of bNOS-immunoreactive neurons in the mouse retina, J. Comp. Neurol., 518, 2456, 10.1002/cne.22347 · DOI
  43. Peachey, 2003, Electrophysiological analysis of visual function in mutant mice, Doc. Ophthalmol., 107, 13, 10.1023/A:1024448314608 · DOI
  44. Przedborski, 1996, Role of neuronal nitric oxide in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced dopaminergic neurotoxicity, Proc. Natl. Acad. Sci. U.S.A., 93, 4565, 10.1073/pnas.93.10.4565 · DOI
  45. Qi, 2014, Rotenone and paraquat perturb dopamine metabolism: a computational analysis of pesticide toxicity, Toxicology, 315, 92, 10.1016/j.tox.2013.11.003 · DOI
  46. Sener, 2001, Visual evoked potentials in Parkinson’s disease-correlation with clinical involvement, Clin. Neurol. Neurosurg., 103, 147, 10.1016/S0303-8467(01)00130-5 · DOI
  47. Smeyne, 2002, Method for culturing postnatal substantia nigra as an in vitro model of experimental Parkinson’s disease, Brain Res. Brain Res. Protoc., 9, 105, 10.1016/S1385-299X(02)00117-4 · DOI
  48. Soulere, 2007, An expeditious synthesis of 4-hydroxy-2E-nonenal (4-HNE), its dimethyl acetal and of related compounds, Chem. Phys. Lipids, 150, 239, 10.1016/j.chemphyslip.2007.07.003 · DOI
  49. Strain, 1993, Flash and pattern reversal visual evoked potentials in C57BL/6J and B6CBAF1/J mice, Brain Res. Bull., 32, 57, 10.1016/0361-9230(93)90319-7 · DOI
  50. Tieu, 2003, Nitric oxide and reactive oxygen species in Parkinson’s disease, IUBMB Life, 55, 329, 10.1080/1521654032000114320 · DOI
  51. Tran, 2001, Amyloid beta-peptide induces nitric oxide production in rat hippocampus: association with cholinergic dysfunction and amelioration by inducible nitric oxide synthase inhibitors, FASEB J., 15, 1407, 10.1096/fj.00-0719fje · DOI
  52. Vielma, 2012, Nitric oxide signaling in the retina: what have we learned in two decades?, Brain Res., 1430, 112, 10.1016/j.brainres.2011.10.045 · DOI
  53. Wichmann, 2003, Pathophysiology of Parkinson’s disease: the MPTP primate model of the human disorder, Ann. N. Y. Acad. Sci., 991, 199, 10.1111/j.1749-6632.2003.tb07477.x · DOI
  54. Yokoyama, 2011, Neuropharmacological approach against MPTP (1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine)-induced mouse model of Parkinson’s disease, Acta Neurobiol. Exp. (Wars), 71, 269, 10.55782/ane-2011-1847 · DOI
  55. Zhou, 2009, Neuronal nitric oxide synthase: structure, subcellular localization, regulation, and clinical implications, Nitric Oxide, 20, 223, 10.1016/j.niox.2009.03.001 · DOI

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Metadata

Authors
Aras, S., Tanriover, G., Aslan, M., Yargicoglu, P., & Agar, A.
Affiliations
Akdeniz University (TR)
Venue
Neurochemistry International
Publisher
Elsevier BV
Published
2014-06
Volume
72
Pages
48-57
ISSN
0197-0186 (ISSN-L)
OpenAlex
W2046291010
Cited by
30
References
1
Citations by year
2026: 3 · 2025: 2 · 2023: 5 · 2022: 3 · 2021: 4 · 2020: 1 · 2019: 3 · 2017: 1 · 2016: 3 · 2015: 3 · 2014: 2
FWCI
1.96
Type
journal article
Language
en
Open access
closed
Locations
  • Neurochemistry International (publishedVersion)
  • PubMed (publishedVersion)
Funders
Akdeniz Üniversitesi
Topics
  • Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Receptors and Signaling
  • Life Sciences › Neuroscience › Neurology › Neuroprotection in Cerebral Ischemia
Keywords
nitric oxide, visual evoked potentials, MPTP-induced parkinsonism, Parkinson's disease, neuronal nitric oxide synthase, inducible nitric oxide synthase, 7-nitroindazole, S-methylisothiourea, dopaminergic neuron death, substantia nigra, lipid peroxidation, apoptosis, caspase-3, 4-hydroxynonenal, nitrite/nitrate, VEP latency, neuroprotection
MeSH terms
Aldehydes, Animals, Evoked Potentials, Visual, Male, Mice, Inbred C57BL, Motor Activity, Nitric Oxide, Psychomotor Performance, Tyrosine 3-Monooxygenase, Lipid Peroxidation, Nitric Oxide Synthase, MPTP Poisoning, Mice, Caspase 3

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