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Differential Vulnerability to Excitatory Amino Acid-Induced Toxicity and Selective Neuronal Loss in Neurodegenerative Diseases

Published online by Cambridge University Press:  18 September 2015

John H. Weiss
Affiliation:
Department of Neurology H-3160, Stanford University Medical Centre, Stanford
Dennis W. Choi*
Affiliation:
Department of Neurology H-3160, Stanford University Medical Centre, Stanford
*
Department of Neurology H-3160, Stanford University Medical Centre, Stanford, California, U.S.A. 94305
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Abstract:

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Neurodegenerative diseases are characterized by selective degeneration of certain biochemically distinct subpopulations of central neurons. Studies of the intrinsic vulnerability of such neurons to injury by excitatory amino acids in vitro, as well as study of neurologic syndromes produced in animals or humans by ingestion of environmental excitatory amino acid neurotoxins may suggest a link between excitotoxicity, and the pathogenesis of certain neurodegenerative diseases.

Type
Research Article
Copyright
Copyright © Canadian Neurological Sciences Federation 1991

References

REFERENCES

1.Rothman, SM, Olney, JW. Glutamate and the pathophysiology of hypoxic-ischemic brain damage. Ann Neurol 1986; 19: 105111.CrossRefGoogle ScholarPubMed
2.Choi, DW. Glutamate neurotoxicity and diseases of the nervous system. Neuron 1988; 1: 623634.CrossRefGoogle ScholarPubMed
3.Watkins, JC, Olverman, HJ. Agonists and antagonists for excitatory amino acid receptors. Trends Neurosci 1987; 10: 265272.CrossRefGoogle Scholar
4.Choi, DW, Koh, J, Peters, S. Pharmacology of glutamate neurotoxicity in cortical cell culture: attenuation by NMDA antagonists. J Neurosci 1988; 8: 185196.CrossRefGoogle ScholarPubMed
5.Michaels, RL, Rothman, SM. Glutamate neurotoxicity in vitro: Antagonist pharmacology and intracellular calcium concentrations. J Neurosci 1990; 10: 283292.CrossRefGoogle ScholarPubMed
6.Koh, J, Goldberg, MP, Hartley, DM, et al. Non-NMDA receptor-mediated neurotoxicity in cortical culture. J Neurosci 1990; 10: 693705.CrossRefGoogle ScholarPubMed
7.McGeer, EG, McGeer, PL. Duplication of biochemical changes of Huntington’s chorea by intrastriatal injections of glutamic and kainic acids. Nature 1976; 263: 517519.CrossRefGoogle ScholarPubMed
8.Coyle, JT, Schwarcz, R. Lesion of striatal neurones with kainic acid provides a model for Huntington’s chorea. Nature 1976; 263: 244246.CrossRefGoogle Scholar
9.Ferrante, RJ, Kowall, NW, Beal, MF, et al. Selective sparing of a class of striatal neurons in Huntington–s disease. Science 1985; 230: 561563.CrossRefGoogle ScholarPubMed
10.Beal, MF, Kowall, NW, Ellison, DW, et al. Replication of the neurochemical characteristics of Huntington’s disease by quinolinic acid. Nature 1986; 321: 168171.CrossRefGoogle ScholarPubMed
11.Schwarcz, R, Whetsell, WO Jr, Mangano, RM. Quinolinic acid: an endogenous metabolite that produces axon-sparing lesions in rat brain. Science 1983; 219: 316318.CrossRefGoogle ScholarPubMed
12.Davies, SW, Roberts, PJ. No evidence for preservation of somato-statin-containing neurons after intrastriatal injections of quinolinic acid. Nature 1987; 327: 326329.CrossRefGoogle ScholarPubMed
13.Boegman, RJ, Parent, A. Differential sensitivity of neuropeptide Y, somatostatin and NADPH-diaphorase containing neurons in rat cortex and striatum to quinolinic acid. Brain Res 1988; 445: 358362.CrossRefGoogle ScholarPubMed
14.Koh, J, Peters, S, Choi, DW. Neurons containing NADPH-diaphorase are selectively resistant to quinolinate toxicity. Science 1986; 234: 7376.CrossRefGoogle ScholarPubMed
15.Koh, J, Choi, DW. Cultured striatal neurons containing NADPH-diaphorase or acetylcholinesterase are selectively resistant to injury by NMDA receptor agonists. Brain Res 1988; 446: 374378.CrossRefGoogle ScholarPubMed
16.Beal, MF, Kowall, NW, Swartz, KJ, et al. Differential sparing of somatostatin-neuropeptide Y and cholinergic neurons following striatal excitotoxin lesions. Synapse 1989; 3: 3847.CrossRefGoogle ScholarPubMed
17.Koh, J, Choi, DW. Vulnerability of cultured cortical neurons to damage by excitotoxins: differential susceptibility of neurons containing NADPH-diaphorase. J Neurosci 1988; 8: 21532163.CrossRefGoogle ScholarPubMed
18.Young, AB, Greenamyre, JT, Hollingsworth, D, et al. NMDA receptor losses in putamen from patients with Huntington’s Disease. Science 1988; 241: 981983.CrossRefGoogle ScholarPubMed
19.Plaitakis, A, Caroscio, JT. Abnormal glutamate metabolism in amyotrophic lateral sclerosis. Ann Neurol 1987; 22: 575579.CrossRefGoogle ScholarPubMed
20.Hugon, J, Tabaraud, F, Rigaud, M, et al. Glutamate dehydrogenase and aspartate aminotransferase in leukocytes of patients with motor neuron disease. Neurology 1989; 39: 956958.CrossRefGoogle ScholarPubMed
21.Rothstein, JD, Tsai, G, Kuncl, RW, et al. Abnormal excitatory amino acid metabolism in amyotrophic lateral sclerosis. Ann Neurol 1990; 28: 1825.CrossRefGoogle ScholarPubMed
22.Watkins, JC, Curtis, DR, Biscoe, TJ. Central effects of beta-N-oxalyl-alpha, beta-diaminopropionic acid and other lathyrus factors. Nature 1966; 211: 637.Google ScholarPubMed
23.Olney, JW, Misra, CH, Rhee, V. Brain and retinal damage from lathyrus excitotoxin, beta-N-oxalyl-L- alpha, beta-diaminopropionic acid. Nature 1976; 264: 659661.CrossRefGoogle ScholarPubMed
24.Spencer, PS, Ludolph, A, Dwivedi, MP, et al. Lathyrism: evidence for role of the neuroexcitatory aminoacid BOAA. Lancet 1986; 2: 10661067.CrossRefGoogle ScholarPubMed
25.Ross, SM, Seelig, M, Spencer, PS. Specific antagonism of excitotoxic action of “uncommon” amino acids assayed in organotypic mouse cortical cultures. Brain Res 1987; 425: 120127.CrossRefGoogle ScholarPubMed
26.Bridges, RJ, Stevens, DR, Kahle, JS, et al. Structure-function studies on N-oxalyl-diamino-dicarboxylic acids and excitatory amino acid receptors: evidence that beta-L-ODAP is a selective non-NMDA agonist. J Neurosci 1989; 9: 20732079.CrossRefGoogle ScholarPubMed
27.Arnold, A, Edgren, DC, Palladino, VS. Amyotrophic lateral sclerosis, fifty cases observed on Guam. J Nerv Ment Dis 1953; 114: 135139.CrossRefGoogle Scholar
28.Hirano, A, Kurland, LT, Krooth, RS, et al. Parkinsonism-dementia complex, an endemic disease on the island of Guam. I. Clinical Features. Brain 1961; 84: 641661.CrossRefGoogle ScholarPubMed
29.Hirano, A, Malamud, N, Kurland, LT. Parkinsonism-dementia complex, an endemic disease on the island of Guam. II. Pathological Features. Brain 1961; 84: 662680.CrossRefGoogle ScholarPubMed
30.Plato, CC, Garruto, RM, Fox, KM, et al. Amyotrophic lateral sclerosis and Parkinsonism-dementia on Guam: A 25-year prospective case-control study. Am J Epidemiol 1986; 124: 643656.CrossRefGoogle ScholarPubMed
31.Spencer , PS, Nunn, PB, Hugon, J, et al. Guam amyotrophic lateral sclerosis-Parkinsonism-dementia linked to a plant excitant neurotoxin. Science 1987; 237: 517522.CrossRefGoogle ScholarPubMed
32.Polsky, FI, Nunn, PB, Bell, EA. Distribution and toxicity of alpha-amino-beta-methylaminopropionic acid. Fed Proc 1972; 31: 4731475.Google ScholarPubMed
33.Weiss, JH, Choi, DW. Beta-N-methylamino-L-alanine neurotoxicity: requirement for bicarbonate as a cofactor. Science 1988; 241: 973975.CrossRefGoogle ScholarPubMed
34.Mroz, EA. Possible role of carbamates in neurotoxicity and neuro-transmitter inactivation. Science 1989; 243: 1615.CrossRefGoogle Scholar
35.Weiss, JH, Koh, J, Choi, DW. Neurotoxicity of beta-N-methylamino-L-alanine (BMAA) and beta-N-oxalylamino-L-alanine (BOAA) on cultured cortical neurons. Brain Res 1989; 497: 6471.CrossRefGoogle ScholarPubMed
36.Richter, KE, Mena, EE. L-beta methylaminoalanine inhibits [3H]glu-tamate binding in the presence of bicarbonate ions. Brain Res 1989; 492: 385388.CrossRefGoogle ScholarPubMed
37.Debonnel, G, Beauchcsne, L, De Montigny, C. Domoic acid, the alleged “mussel toxin”, might produce its neurotoxic effect through kainate receptor activation: an electrophysiologic study in the rat dorsal hippocampus. Can J Physiol Pharmacol 1989; 67: 2933.CrossRefGoogle Scholar
38.Perl, TM, Bedard, L, Kosaisky, T, et al. An outbreak of toxic encephalopathy caused by eating mussels contaminated with domoic acid. New Eng J Med 1990; 322: 17751780.CrossRefGoogle ScholarPubMed
39.Teitelbaum, JS, Zatorre, RJ, Carpenter, S, et al. Neurologic sequelae of domoic acid intoxication due to the ingestion of contaminated mussels. New Eng J Med 1990; 322: 17811787.CrossRefGoogle Scholar
40.Biscoe, TJ, Evans, RH, Headley, PM, et al. Structure-activity relations of excitatory amino acids on frog and rat spinal neurones. Br J Pharmacol 1976; 58: 373382.CrossRefGoogle ScholarPubMed
41.O’Brien, RJ, Fischbach, GD. Modulation of embryonic chick motoneuron glutamate sensitivity by interneurons and agonists. J Neurosci 1986; 6: 32903296.CrossRefGoogle ScholarPubMed
42.Hugon, J, Vallat, JN, Spencer, PS, et al. Kainic acid induces early and delayed degenerative neuronal changes in rat spinal cord. Neurosci Lett 1989; 104: 258262.CrossRefGoogle ScholarPubMed
43.Greenamyre, JT, Young, AB. Excitatory amino acids and Alzheimer’s disease. Neurobiol Aging 1989; 10: 593602.CrossRefGoogle ScholarPubMed
44.Cotman, CW, Geddes, JW, Bridges, RJ, Monaghan, DT. N-methyl-D-aspartate receptors in Alzheimer’s disease. Neurobiol Aging 1989; 10: 603605.CrossRefGoogle Scholar
45.Choi, DW. Non-NMDA receptor-mediated neuronal injury in Alzheimer’s disease? Neurobiol Aging 1989; 10: 605606.CrossRefGoogle ScholarPubMed
46.Davies, P, Katzman, R, Terry, RD. Reduced somatostatin-like immunoreactivity in cerebral cortex from cases of Alzheimer disease and Alzheimer senile dementa. Nature 1980; 288: 279280.CrossRefGoogle ScholarPubMed
47.Rossor, MN, Emson, PC, Mountjoy, CQ, et al. Reduced amounts of immunoreactive somatostatin in the temporal cortex in senile dementia of Alzheimer type. Neurosci Lett 1980; 20: 373377.CrossRefGoogle ScholarPubMed
48.Chan-Palay, V. Somatostatin immumoreactive neurons in the human hippocampus and cortex shown by immunogold/silver intensification on vibratome sections: coexistence with neuropeptide Y neurons, and effects in Alzheimer-type dementia. J Comp Neurol 1987; 260: 201223.CrossRefGoogle Scholar
49.Arai, H, Emson, PC, Mountjoy, CQ, et al. Loss of parvalbumin-immunoreactive neurons from cortex in Alzheimer-type dementia. Brain Res 1987; 418: 164169.CrossRefGoogle ScholarPubMed
50.Weiss, JH, Koh, J, Baimbridge, KG, et al. Cortical neurons containing somatostatin or parvalbumin-like immunoreactivity are atyp-ically vulnerable to excitotoxic injury in vitro. Neurology 1990; 40: 12881292.CrossRefGoogle ScholarPubMed
51.Mattson, MP. Antigenic changes similar to those seen in neurofibrillary tangles are elicited by glutamate and Ca2+ influx in cultured hippocampal neurons. Neuron 1990; 2: 105117.CrossRefGoogle Scholar
52.Olney, JW, Zorumski, C, Price, MT, Labruyere, J. L-cysteine, a bicarbonate-sensitive endogenous excitotoxin. Science 1990; 248: 596599.CrossRefGoogle ScholarPubMed
53.Choi, DW. Calcium-mediated neurotoxicity: relationship to specific channel types and role in ischemic damage. Trends Neurosci 1988; 11: 465469.CrossRefGoogle ScholarPubMed
54.Campbell, LW, Hao, SY, Landfield, PW. Aging-related increases in L-like calcium currents in rat hippocampal slices. Soc Neurosci Abstr 1989; 15: 260.Google Scholar
55.Kerr, DS, Campbell, LW, Hao, SY, Landfield, PW. Corticosteroid modulation of hippocampal potentials: increased effect with aging. Science 1989; 245: 15051509.CrossRefGoogle ScholarPubMed
56.Choi, DW. Methods for antagonizing glutamate neurotoxicity. Cerebrovasc Brain Metab Rev 1990; 2: 105147.Google ScholarPubMed