3-Nitropropionic acid exacerbates N-methyl-d-aspartate toxicity in striatal culture by multiple mechanisms
暂无分享,去创建一个
R. Gross | J. T. Greenamyre | S. Sheu | J. Greene | S. Sheu | J. Greenamyre | J. Greene | J. T. Greenamyre | R.A Gross | J. Greenamyre
[1] J. Passonneau,et al. The enzymatic measurement of adenine nucleotides and P-creatine in picomole amounts. , 1981, Analytical biochemistry.
[2] L. Nowak,et al. Magnesium gates glutamate-activated channels in mouse central neurones , 1984, Nature.
[3] R. Tsien,et al. A new generation of Ca2+ indicators with greatly improved fluorescence properties. , 1985, The Journal of biological chemistry.
[4] J. Olney,et al. Excitotoxity and the NMDA receptor , 1987, Trends in Neurosciences.
[5] D. Choi,et al. Glutamate neurotoxicity and diseases of the nervous system , 1988, Neuron.
[6] A. Novelli,et al. Glutamate becomes neurotoxic via the N-methyl-d-aspartate receptor when intracellular energy levels are reduced , 1988, Brain Research.
[7] M. Blaustein. Calcium transport and buffering in neurons , 1988, Trends in Neurosciences.
[8] M. J. Gallagher,et al. Diffusible factor(s) from adult rat sciatic nerve increases cell number and neurite outgrowth of cultured embryonic ventral mesencephalic tyrosine hydroxylase‐positive neurons , 1990, Journal of neuroscience research.
[9] M. Erecińska,et al. Relationships between the neuronal sodium/potassium pump and energy metabolism. Effects of K+, Na+, and adenosine triphosphate in isolated brain synaptosomes , 1990, The Journal of general physiology.
[10] M. Poenie. Alteration of intracellular Fura-2 fluorescence by viscosity: a simple correction. , 1990, Cell calcium.
[11] P. Lipton,et al. Mechanisms of intracellular calcium accumulation in the CA1 region of rat hippocampus during anoxia in vitro. , 1990, Stroke.
[12] G. Zeevalk,et al. Mechanisms underlying initiation of excitotoxicity associated with metabolic inhibition. , 1991, The Journal of pharmacology and experimental therapeutics.
[13] J. Dubinsky,et al. Intracellular calcium concentrations during "chemical hypoxia" and excitotoxic neuronal injury , 1991, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[14] J. Arreola,et al. Ca2+ current and Ca2+ transients under action potential clamp in guinea pig ventricular myocytes. , 1991, The American journal of physiology.
[15] S. Rothman. Excitotoxins: Possible Mechanisms of Action a , 1992, Annals of the New York Academy of Sciences.
[16] G. Zeevalk,et al. Evidence that the Loss of the Voltage‐Dependent Mg2+ Block at the N‐Methyl‐D‐Aspartate Receptor Underlies Receptor Activation During Inhibition of Neuronal Metabolism , 1992, Journal of neurochemistry.
[17] D. Choi. Excitotoxic cell death. , 1992, Journal of neurobiology.
[18] M. Beal,et al. Does impairment of energy metabolism result in excitotoxic neuronal death in neurodegenerative illnesses? , 1992, Annals of neurology.
[19] R. Albin,et al. Alternative excitotoxic hypotheses , 1992, Neurology.
[20] Samuel Thayer,et al. Glutamate-induced calcium transient triggers delayed calcium overload and neurotoxicity in rat hippocampal neurons , 1992, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[21] B. Rosen,et al. Age‐Dependent Vulnerability of the Striatum to the Mitochondrial Toxin 3‐Nitropropionic Acid , 1993, Journal of neurochemistry.
[22] J. Coyle,et al. Oxidative stress, glutamate, and neurodegenerative disorders. , 1993, Science.
[23] D. Choi,et al. Glutamate receptor-induced 45Ca2+ accumulation in cortical cell culture correlates with subsequent neuronal degeneration , 1993, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[24] M. Weller,et al. 3-Nitropropionic acid is an indirect excitotoxin to cultured cerebellar granule neurons. , 1993, European journal of pharmacology.
[25] Elsdon Storey,et al. Excitotoxin Lesions in Primates as a Model for Huntington's Disease: Histopathologic and Neurochemical Characterization , 1993, Experimental Neurology.
[26] B. Hyman,et al. Neurochemical and histologic characterization of striatal excitotoxic lesions produced by the mitochondrial toxin 3-nitropropionic acid , 1993, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[27] R. Porter,et al. Inhibition of Succinate Dehydrogenase by Malonic Acid Produces an “Excitotoxic” Lesion in Rat Striatum , 1993, Journal of neurochemistry.
[28] O. Isacson,et al. Mitochondrial Impairment Reduces the Threshold for in Vivo NMDA-Mediated Neuronal Death in the Striatum , 1993, Experimental Neurology.
[29] B. Hyman,et al. Age‐Dependent Striatal Excitotoxic Lesions Produced by the Endogenous Mitochondrial Inhibitor Malonate , 1993, Journal of neurochemistry.
[30] I. Reynolds,et al. Glutamate-induced intracellular calcium changes and neurotoxicity in cortical neuronsin vitro: Effect of chemical ischemia , 1994, Neuroscience.
[31] B. Rosen,et al. Malonate produces striatal lesions by indirect NMDA receptor activation , 1994, Brain Research.
[32] M. Beal,et al. Bioenergetic and oxidative stress in neurodegenerative diseases. , 1995, Life sciences.
[33] M. Beal,et al. Aging, energy, and oxidative stress in neurodegenerative diseases , 1995, Annals of neurology.
[34] G. Zeevalk,et al. NMDA Receptor Involvement in Toxicity to Dopamine Neurons In Vitro Caused by the Succinate Dehydrogenase Inhibitor 3‐Nitropropionic Acid , 1995, Journal of neurochemistry.
[35] M. Goldberg,et al. Abnormal calcium homeostasis and mitochondrial polarization in a human encephalomyopathy. , 1995, Proceedings of the National Academy of Sciences of the United States of America.
[36] J. Greene,et al. Exacerbation of NMDA, AMPA, and l‐Glutamate Excitotoxicity by the Succinate Dehydrogenase Inhibitor Malonate , 1995, Journal of neurochemistry.
[37] M. Beal,et al. Chronic mitochondrial energy impairment produces selective striatal degeneration and abnormal choreiform movements in primates. , 1995, Proceedings of the National Academy of Sciences of the United States of America.
[38] G. Zeevalk,et al. Relative vulnerability of dopamine and GABA neurons in mesencephalic culture to inhibition of succinate dehydrogenase by malonate and 3-nitropropionic acid and protection by NMDA receptor blockade. , 1995, The Journal of pharmacology and experimental therapeutics.
[39] R. White,et al. Mitochondria and Na+/Ca2+ exchange buffer glutamate-induced calcium loads in cultured cortical neurons , 1995, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[40] I. Kaneko,et al. Suppression of Mitochondrial Succinate Dehydrogenase, a Primary Target of β‐Amyloid, and Its Derivative Racemized at Ser Residue , 1995, Journal of neurochemistry.
[41] M. Mattson,et al. Amyloid beta-peptide impairs ion-motive ATPase activities: evidence for a role in loss of neuronal Ca2+ homeostasis and cell death , 1995, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[42] J. Greene,et al. Characterization of the Excitotoxic Potential of the Reversible Succinate Dehydrogenase Inhibitor Malonate , 1995, Journal of neurochemistry.
[43] Greenamyre Jt,et al. Bioenergetics and glutamate excitotoxicity. , 1996 .
[44] S. Budd,et al. A Reevaluation of the Role of Mitochondria in Neuronal Ca2+ Homeostasis , 1996, Journal of neurochemistry.
[45] R. Delorenzo,et al. Ischemia‐Induced Inhibition of Calcium Uptake into Rat Brain Microsomes Mediated by Mg2+/Ca2+ ATPase , 1997, Journal of neurochemistry.
[46] P. Calabresi,et al. Opposite Membrane Potential Changes Induced by Glucose Deprivation in Striatal Spiny Neurons and in Large Aspiny Interneurons , 1997, The Journal of Neuroscience.
[47] Robert E. Davis,et al. Altered Calcium Homeostasis in Cells Transformed by Mitochondria from Individuals with Parkinson's Disease , 1997, Journal of neurochemistry.