Glutathione In The Nervous SystemChristopher Ari Shaw The goal of this text is to focus readers attention on three major areas; the origin and localization of GSH in the nervous system; the multiple effects of GSH on neural health activity; and the potential for alterations on GSH status to lead to neurological damage of the type observed in amyotrophic lateral sclerosis, Parkinson's disease and other neurological disorders. The text also touches upon the additional roles of the antoxidant GSH, including possible neurotransmitter action, redox modulation of ionotropic receptor function, and neuroprotection against exicitoxic actions of glutamate. |
Contents
Multiple Roles of Glutathione in the Nervous System | 3 |
The Discovery of the GSH Receptor in Hydra and | 25 |
CarrierMediated GSH Transport at the BloodBrain | 45 |
Production Characterization | 63 |
Role of Astrocytes in Maintaining Cerebral Glutathione | 91 |
Glutathione and the Regulation of Apoptosis in | 117 |
Possible Modulation by Glutathione of Glutamatergic | 137 |
Excitatory Actions of GSH on Neocortex | 197 |
Glutathione in Brain Aging and Neurodegenerative Disorders | 231 |
The Glutathione Redox State and Zinc Mobilization from | 257 |
Glutathione Release and Nitrosoglutathione Presence in | 275 |
The Role of Altered Glutathione Status in the Development | 287 |
FreeRadical Toxicity in Amyotrophic Lateral Sclerosis | 343 |
Is Glutathione | 355 |
| 385 | |
Medicinal Chemistry of Glutathione and Glutathione Analogs | 217 |
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Common terms and phrases
activity agonists amino acids AMPA antagonists antioxidant apoptosis astrocytes Benzi binding sites Biochemical Biological Brain Research Ca2+ cell death cellular complex concentrations cortex cortical CySH cysteine damage disulfide dopamine dopaminergic Dryhurst effects enzymes excitatory excitotoxic feeding response free radicals function glial cells glutamate receptors glutamatergic glutathione depletion glutathione peroxidase glycine GSH and GSSG GSH depletion GSH receptor GSH transport Hjelle hydra increased induced inhibition inhibitor intracellular ionotropic Janáky Jenner Journal of Neurochemistry Lenhoff mechanisms Meister metabolism mitochondrial modulation Molecular MPP+ neural Neurochemistry neurodegenerative Neurology neuromelanin neurons Neuroscience Letters neurotoxicity neurotransmitter NH3+ nitric oxide NMDA receptor Ogita Ottersen oxidative stress oxidized glutathione oxygen Parkinson's disease Parkinsonian pathway patients peptides Pharmacology potential protein rat brain reaction reactive redox reduced glutathione reductase release Riederer role Shaw Sian specific striatum studies substantia nigra superoxide synaptic membranes synthesis thiol tissue toxicity uptake vitro vivo y-glutamyl Yoneda zinc
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Page 379 - Gurney, ME, Pu, H., Chiu, AY, Dal Canto, MC, Polchow, CY, Alexander, DD, Caliendo, J., Hentati, A., Kwon, YW, Deng, HX, Chen, W., Zhai, P., Sufit, RL, and Siddique, T.
Page 376 - Apoptosis and necrosis: two distinct events induced, respectively, by mild and intense insults with N-methyl-D-aspartate or nitric oxide/superoxide in cortical cell cultures.
Page 381 - NA, Vaillancourt, JP, Ding, CK, Gallant, M., Gareau, Y, Griffin, PR, Labelle, M., Lazebnik, YA, Munday, NA, Raju, SM, Smulson, ME, Yamin, T.-T, Yu, VL, and Miller, DK (1995) Identification and inhibition of the ICE/CED-3 protease necessary for mammalian apoptosis, Nature 376, 37-43.