The DOI matches its Crossref record; 44 of the 44 references it cites were found in a registry or an index.
Blockade of neuronal nitric oxide synthase protects against excitotoxicity in vivo
Open accessAbstract
Nitric oxide may be a key mediator of excitotoxic neuronal injury in the central nervous system. We examined the effects of the neuronal nitric oxide synthase inhibitor 7-nitroindazole (7-NI) on excitotoxic striatal lesions. 7-NI significantly attenuated lesions produced by intrastriatal injections of NMDA, but not kainic acid or alpha-amino-3- hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) 7-NI attenuated secondary striatal excitotoxic lesions produced by the succinate dehydrogenase inhibitor malonate, and the protection was reversed by L- arginine but not by D-arginine, 7-NI produced nearly complete protection against striatal lesions produced by systemic administration of 3-nitropropionic acid (3-NP), another succinate dehydrogenase inhibitor, 7-NI protected against malonate induced decreases in ATP, and increases in lactate, as assessed by 1H magnetic resonance spectroscopy. 7-NI had no effects on spontaneous electrophysiologic activity in the striatum in vivo, suggesting that its effects were not mediated by an interaction with excitatory amino acid receptors. 7-NI attenuated increases in hydroxyl radical, 8-hydroxy-2-deoxyguanosine and 3-nitrotyrosine generation in vivo, which may be a consequence of peroxynitrite formation. The present results implicate neuronal nitric oxide generation in the pathogenesis of both direct and secondary excitotoxic neuronal injury in vivo. As such they suggest that neuronal nitric oxide synthase inhibitors may be useful in the treatment of neurologic diseases in which excitotoxic mechanisms play a role.
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Nitric oxide mediates glutamate neurotoxicity in primary cortical cultures.
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Effects of Cerebral Ischemia in Mice Deficient in Neuronal Nitric Oxide Synthase
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Peroxynitrite-mediated tyrosine nitration catalyzed by superoxide dismutase
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Extensive Nitration of Protein Tyrosines in Human Atherosclerosis Detected by Immunohistochemistry
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Nitric Oxide Activation of Poly(ADP-Ribose) Synthetase in Neurotoxicity
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Gases as biological messengers: nitric oxide and carbon monoxide in the brain
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The Therapeutic Potential of Poly(ADP-Ribose) Polymerase Inhibitors
Virág, L., & Szabó, C. (2002) · Pharmacological Reviews · doi:10.1124/pr.54.3.375 · Cited by 1,373
13 reasons why the brain is susceptible to oxidative stress
Cobley, J. N., Fiorello, M. L., & Bailey, D. M. (2018) · Redox Biology · doi:10.1016/j.redox.2018.01.008 · Cited by 1,215
Klivenyi, P., Andreassen, O. A., Ferrante, R. J., Dedeoglu, A., Mueller, G., Lancelot, E., Bogdanov, M., Andersen, J. K., Jiang, D., & Beal, M. F. (2000) · The Journal of Neuroscience · doi:10.1523/jneurosci.20-01-00001.2000 · Cited by 1,111
Self-citationThe Role of Excitotoxicity in Neurodegenerative Disease
Doble, A. (1999) · Pharmacology & Therapeutics · doi:10.1016/s0163-7258(98)00042-4 · Cited by 723
Hensley, K., Maidt, M. L., Yu, Z., Sang, H., Markesbery, W. R., & Floyd, R. A. (1998) · The Journal of Neuroscience · doi:10.1523/jneurosci.18-20-08126.1998 · Cited by 507
Metadata
- Authors
- Schulz, J., Matthews, R., Jenkins, B., Ferrante, R., Siwek, D., Henshaw, D., Cipolloni, P., Mecocci, P., Kowall, N., & Rosen, B.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 1995-12-01
- Volume
- 15
- Issue
- 12
- Pages
- 8419-8429
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W1569800962
- Cited by
- 281
- References
- 44
- FWCI
- 9.15
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Schulz, J., Matthews, R., Jenkins, B., Ferrante, R., Siwek, D., Henshaw, D., Cipolloni, P., Mecocci, P., Kowall, N., & Rosen, B. (1995). Blockade of neuronal nitric oxide synthase protects against excitotoxicity in vivo. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.15-12-08419.1995
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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