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[Neuronal cell death in neurodegenerative disorders and oxidative stress].
Rinsho Shinkeigaku. 1999 Jan; 39(1):4-6.RS

Abstract

Mechanisms of the process of neuronal degeneration in neurodegenerative disorders such as amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), and Alzheimer's disease (AD) remain unsolved. Oxidative stress might be a possible mechanism of neuronal cell death. Glutamate is an excitatory amino acid and its excessive release can cause intracellular calcium influx, activation of calcium-dependent enzymes such as nitric oxide (NO) synthase (NOS), and production of toxic oxygen radicals. Excessive release of glutamate, therefore, can be used as a model of experimental oxidative stress. Continuous exposure to low levels of glutamate potentiates selective motor neuronal death mediated by NO, which inversely protects nonmotor neurons through the guanylyl cyclase-cGMP cascade. Mesencephalic dopaminergic neurons are resistant to cytotoxicity induced by NO. The protecting mechanism from NO neurotoxicity in dopaminergic neurons is based on inhibition of conversion of NO to peroxynitrite anion, and is possibly due to suppression of superoxide anion production. Dopamine D 2 agonists provide protection mediated not only by the inhibition of dopamine turnover but also via D 2-type dopamine receptor stimulation and the subsequent synthesis of proteins that scavenge free radicals. In addition, nicotinic receptor stimulation may be able to protect neurons from oxidative stress induced by A beta.

Authors+Show Affiliations

Department of Neurology, Faculty of Medicine, Kyoto University.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

English Abstract
Journal Article
Review

Language

jpn

PubMed ID

10377784

Citation

Shimohama, S, et al. "[Neuronal Cell Death in Neurodegenerative Disorders and Oxidative Stress]." Rinsho Shinkeigaku = Clinical Neurology, vol. 39, no. 1, 1999, pp. 4-6.
Shimohama S, Sawada H, Kihara T, et al. [Neuronal cell death in neurodegenerative disorders and oxidative stress]. Rinsho Shinkeigaku. 1999;39(1):4-6.
Shimohama, S., Sawada, H., Kihara, T., & Urushitani, M. (1999). [Neuronal cell death in neurodegenerative disorders and oxidative stress]. Rinsho Shinkeigaku = Clinical Neurology, 39(1), 4-6.
Shimohama S, et al. [Neuronal Cell Death in Neurodegenerative Disorders and Oxidative Stress]. Rinsho Shinkeigaku. 1999;39(1):4-6. PubMed PMID: 10377784.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Neuronal cell death in neurodegenerative disorders and oxidative stress]. AU - Shimohama,S, AU - Sawada,H, AU - Kihara,T, AU - Urushitani,M, PY - 1999/6/23/pubmed PY - 1999/6/23/medline PY - 1999/6/23/entrez SP - 4 EP - 6 JF - Rinsho shinkeigaku = Clinical neurology JO - Rinsho Shinkeigaku VL - 39 IS - 1 N2 - Mechanisms of the process of neuronal degeneration in neurodegenerative disorders such as amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), and Alzheimer's disease (AD) remain unsolved. Oxidative stress might be a possible mechanism of neuronal cell death. Glutamate is an excitatory amino acid and its excessive release can cause intracellular calcium influx, activation of calcium-dependent enzymes such as nitric oxide (NO) synthase (NOS), and production of toxic oxygen radicals. Excessive release of glutamate, therefore, can be used as a model of experimental oxidative stress. Continuous exposure to low levels of glutamate potentiates selective motor neuronal death mediated by NO, which inversely protects nonmotor neurons through the guanylyl cyclase-cGMP cascade. Mesencephalic dopaminergic neurons are resistant to cytotoxicity induced by NO. The protecting mechanism from NO neurotoxicity in dopaminergic neurons is based on inhibition of conversion of NO to peroxynitrite anion, and is possibly due to suppression of superoxide anion production. Dopamine D 2 agonists provide protection mediated not only by the inhibition of dopamine turnover but also via D 2-type dopamine receptor stimulation and the subsequent synthesis of proteins that scavenge free radicals. In addition, nicotinic receptor stimulation may be able to protect neurons from oxidative stress induced by A beta. SN - 0009-918X UR - https://www.unboundmedicine.com/medline/citation/10377784/[Neuronal_cell_death_in_neurodegenerative_disorders_and_oxidative_stress]_ L2 - https://medlineplus.gov/degenerativenervediseases.html DB - PRIME DP - Unbound Medicine ER -
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