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Speculations on Disease States Induced by Excitatory Amino Acids

Published online by Cambridge University Press:  18 September 2015

John Turnbull
John Turnbull*
Affiliation:
Center for the Neurobiology of Learning and Memory, University of California, Irvine, California
*
Center for the Neurobiology of Learning and Memory, University of California, Irvine, Irvine, California, U.S.A. 92717
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Abstract:

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There is much current interest in excitatory amino acids and their receptors because of their postulated involvement in several disorders of the nervous system. They function as neurotransmitters, but can act as neurotoxins in some situations. They have been implicated in the pathogenesis of cerebral hypoxic/ischemic and hypoglycemic damage, in epilepsy, in some degenerative diseases, and in some forms of neurotoxin-induced cerebral dysfunction. These diseases may reflect abnormality in a system which has evolved to provide synaptic plasticity essential for learning and memory. The purpose of this paper is to explore the ramifications of such a hypothesis.

Type
Hypothesis
Information
Canadian Journal of Neurological Sciences , Volume 14 , Issue 2 , May 1987 , pp. 122 - 126
Copyright
Copyright © Canadian Neurological Sciences Federation 1987

References

1.Oleny, JW. Excitotoxins: an overview.In: Excitotoxins. Fuxe, K, Roberts, P, Schwarcz, R, eds. Plenum Press, New York 1983; 82–96.Google Scholar
2.Rothman, SM, Olney, JW. Glutamate and the pathophysiology of hypoxic ischemic brain damage. Ann Neurol 1986; 19: 105–111.CrossRefGoogle ScholarPubMed
3.Rothman, SM. Synaptic activity mediates death of hypoxic neurons. Science 1983; 220: 536–537.CrossRefGoogle ScholarPubMed
4.Rothman, SM. Synaptic release of excitatory amino acid neurotransmitter mediates anoxic neuronal death. J Neurosci 1984; 4: 1884–1891.CrossRefGoogle ScholarPubMed
5.Meldrum, B. Excitatory amino acids and anoxic/ischaemic brain damage. TINS 1985, Feb, 47–48.Google Scholar
6.Wieloch, T, Lindvall, O, Blomqvist, P, Gage, FH. Evidence for amelioration of ischaemic neuronal damage in the hippocampal formation by lesions of the perforant path. Neurol Res 1985; 7: 24–26.CrossRefGoogle ScholarPubMed
7.Simon, RP, Swan, JH, Griffiths, T, Meldrum, BS. Blockade of N-methyl-D-aspartate receptors may protect against ischemic damage in the brain. Science 1984; 266: 850–852.CrossRefGoogle Scholar
8.Schwarcz, R, Meldrum, B. Excitatory amino acid antagonists provide a therapeutic approach to neurological disorders. Lancet 1985, 8447: 140–143.CrossRefGoogle Scholar
9.Croucher, MJ, Collins, JF, Meldrum, BS. Anticonvulsant action of excitatory amino acid antagonists. Science 1982; 216: 899–901.CrossRefGoogle ScholarPubMed
10.Savage, DD, Werling, LL, Nadler, JV, McNamara, JO. Selective and reversible increase in the number of Quisqualate sensitive glutamate binding sites on hippocampal synaptic membranes after angular bundle kindling. Brain Res 1984; 307: 332–335.CrossRefGoogle ScholarPubMed
11.Fagg, GE. L glutamate, excitatory amino acid receptors and brain function. TINS 1985, May, 207–210.Google Scholar
12.MacDonald, JF, Morris, ME. Lathyrus excitotoxin: mechanism of neuronal excitation by L-2-oxalylamino-3-amino- and L-3-oxalylamino- 2-amino-propionicacid. Exp Brain Res 1984; 57: 158–166.CrossRefGoogle Scholar
13.Brown, AW, Aldridge, WN, Street, BW, Verschoyle, RD. The behavioral and neuropathologic sequelae of intoxication by trimethyltin compounds in the rat. Am J Pathol 1979; 97: 59.Google ScholarPubMed
14.Shoulson, I.Huntington’s disease: anti-neurotoxic therapeutic strategies. In: Excitotoxins. Fuxe, K, Roberts, P, Schwarcz, R, eds. Plenum Press, New York 1983; 343–353.Google Scholar
15.Schwarcz, R, Foster, A, French, AC, Whetsell, WO, Kohler, C.Excitotoxic models for neurodegenerative disorders. Life Sci 1984; 35: 19–32.CrossRefGoogle ScholarPubMed
16.Geddes, JW, Monaghan, DT, Cotman, CW, Lott, IT, Kim, RC, Chui, HC. Plasticity of hippocampal circuitry in Alzheimer’s Disease. Science 1985; 230: 1179–1181.CrossRefGoogle ScholarPubMed
17.Plaitakis, A, Nicklas, WJ, Desnick, RJ. Glutamate dehydrogenase deficiency in three patients with spinocerebellar syndrome.Ann Neurol 1980; 7: 297–303.CrossRefGoogle ScholarPubMed
18.Bliss, TVP, Gardner-Medwin, AT.Long-lasting potentiation of synaptic transmission in the dentate area of the unanaestetized rabbit following stimulation of the perforant path. J Physiol (Lond) 1973; 232: 357–74.CrossRefGoogle ScholarPubMed
19.Douglas, RM, Goddard , GV. Long-term potentiation of the perforant cellpath-granule cell synapse in the rat hippocampus. Brain Res 1975; 86: 205–15.CrossRefGoogle ScholarPubMed
20.Barnes, CA. Memory deficits associated with senescence: a neurophysiological and behavioural study in the rat. J Comp Physiol Psychol 1979; 93: 74–103.CrossRefGoogle ScholarPubMed
21.Morris, RGM, Anderson, E, Lynch, G, Beaudry, M. Selective impairment of learning and blockade of long-term potentiation by an N-methyl-D-aspartate receptor antagonist, AP-5. Nature 1986; 319: 774–776.CrossRefGoogle Scholar
22.Storm-Mathiesen, J. Localisation of neurotransmitter candidates in the brain: the hippocampal formation as a model. Prog Neurobiol 1977; 8: 119.CrossRefGoogle Scholar
23.Dunwiddie, TV, Madison, D, Lynch, GS. Synaptic transmission is required for initiation of long-term potentiation. Brain Res 1978; 150: 413–417.CrossRefGoogle ScholarPubMed
24.Lovinger, DM, Colley, PA, Akers, RF, Nelson, RB, Routtenberg, A. Direct relation of long-term potentiation to phosphorylation of protein Fl, a substrate for membrane protein kinase C. Brain Res 1986; 399: 205–211.CrossRefGoogle Scholar
25.Kaczmarek, LE.The age of onset of Parkinson’s disease. TINS 1987; Jan. 30–34.Google Scholar
26.Lynch, G, Baudry, M.The biochemistry of memory: a new and specific hypothesis. Science 1984; 224: 1057–1063.CrossRefGoogle ScholarPubMed
27.Lynch, G, Larson, J, Kelso, S, Barrionuevo, G, Brown, T.Intracellular injections of EGTA block induction of hippocampal long-term potentiation. Nature {London] 1983; 305: 719–721.Google Scholar
28.Baudry, M, Lynch, G.Regulation of hippocampal glutamate receptors: evidence for the involvement of a calcium activated protease. Proc Natl Acad Sci USA 1980; 77: 2298–2298.CrossRefGoogle ScholarPubMed
29.Baudry, M, Kramer, K, Lynch, G.Irreversibility and time course of calcium stimulated [3H] glutamate binding to rat hippocampal membranes. Brain Res 1983; 270: 142–145.CrossRefGoogle ScholarPubMed
30.Baudry, M, Smith, E, Lynch, G.Influence of temperature, detergents, and enzymes on glutamate receptor binding and its regulation by calcium in rat hippocampal membranes. Mol Pharmacol 1981; 20: 280–286.Google ScholarPubMed
31.Siman, R, Baudry, M, Lynch, G. Purification from synaptosomal plasma membranes of Calpain 1, a thiol protease activated by micromolar calcium concentrations. J Neurochem 1983; 41: 950–956.CrossRefGoogle ScholarPubMed
32.Baldassare, JJ, Bakshian, S, Knipp, MA, Fisher, GJ. Inhibition of fibrinogen receptor expression and serotonin release by leupeptin and antipain. J Biol Chem 1985; 260: 10531–10535.CrossRefGoogle ScholarPubMed
33.Foster, AC, Fagg, GE. Acidic amino acid binding sites in mammalian neuronal membranes: their characteristics and relationship to synaptic receptors. Brain Res Rev 1984; 7: 103–164.CrossRefGoogle Scholar
34.Byrne, JH. Neural and molecular mechanisms underlying information storage in Aplysia: implications for learning and memory. TINS 1985; Nov. 478–482.Google Scholar
35.Crunelli, V, Forda, S, Kelly, JS.Excitatory amino acids in the hippocampus: synaptic physiology and pharmacology. TINS 1985; Jan. 26–30.Google Scholar
36.Goddard, GV, Douglas, RM.Does the engram of kindling model the engram of normal long-term memory? Can J Neurol Sci 1975; 2: 385–394.CrossRefGoogle ScholarPubMed
37.Hughes, JR.Long-term clinical and EEG changes in patients with epilepsy. Arch Neurol 1985; 42: 213–223.CrossRefGoogle ScholarPubMed
38.Griffiths, T, Evans, MC, Meldrum, BS.Temporal lobe epilepsy, excitotoxins, and the mechanism of selective neuronal loss. In: Excitotoxins. Fuxe, K, Roberts, P, Schwarcz, R, eds. Plenum Press, New York 1983; 331–342.Google Scholar
39.Wada, JA.The clinical relevance of kindling: species, brain sites and seizure susceptibility. In: Limbic mechanisms. Livingston, KE, Hornykiewicz, O, eds. Plenum Press 1978; 369–388.CrossRefGoogle Scholar
40.Honey, CR, MacDonald, JF.Phencyclidine and Ketamine block aspartic acid responses. Neurosci L 1985; 61: 135–139.Google ScholarPubMed
41.Rothman, S.The neurotoxicity of excitatory amino acids is produced by passive chloride influx. J Neurosci 1985; 5: 1483–1489.Google Scholar
42.Wieloch, T.Hypoglycemia-induced neuronal damage prevented by an N-methy 1-D-aspartate antagonist. Science 1985; 230: 681–683.Google Scholar