Abstract
In recent years, the possible role(s) of excitatory amino acid (EAA) transmitters in neuropsychiatric disorders has become a topic of considerable interest. Two rather dissimilar hypotheses have evolved: 1) that excess EAA receptor stimulation might be the mechanism underlying certain neurodegenerative disorders; 2) that insufficient EAA receptor stimulation may lead to psychotic processes and/or memory dysfunction. Here evidence relevant to each of these hypotheses will be discussed.
Supported in part by NIMH Research Scientist Award (MH 38894) and a grant from the Washington University/Monsanto Biomedical Research Fund.
This is a preview of subscription content, log in via an institution to check access.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Olney, J.W., Ho, O.L. and Rhee, V. (1971). Cytotoxic effects of acidic and sulphur-containing amino acids on the infant mouse central nervous system. Exp. Brain Res. 14, 61–76.
Olney, J.W., Misra, C.H. and deGubareff, T. (1975). Cysteine-S-sulfate: Brain damaging metabolite in sulfite oxidase deficiency. J. Neuropathol Exp. Neurol. 34, 167–176.
Olney, J. W., Collins, R.C. and Sloviter, R.S. (1986). Excitotoxic mechanisms of epileptic brain damage. In Advances in Neurology, Vol 44, Basic Mechanisms of the Epilepsies: Molecular and Cellular Approaches, Delgado-Escueta, A.V., Ward, A.A., Woodbury, D.M. and Porter, R.J., eds., Raven, New York, pp. 857–878.
Collins, R.C. and Olney, J.W. (1982). Focal cortical seizures cause distant thalamic lesions. Science 218, 177–179.
Olney, J.W., deGubareff, T. and Sloviter, R.S. (1983). “Epileptic” brain damage in rats induced by sustained electrical stimulation of the perforant path. II. Ultrastructural analysis of acute hippocampal pathology. Brain Res. Bull. 10, 699–712.
Labruyere, J., Fuller, T.A., Olney, J.W., Price, M.T., Zorumski, C. and Clifford, D. (1986). Phencyclidine and ketamine protect against kainic acid-induced seizures and seizure-related brain damage. Neurosci. Abst. 12, 344.
Wieloch, T. (1985). Hypoglycemia-induced neuronal damage prevented by an N-methyl-D-aspartate antagonist. Science 230, 681–683.
Rothman, S.M. and Olney, J.W. (1986). Glutamate and the pathophysiology of hypoxic-ischemic brain damage. Ann. Neurol. 19, 105–111.
Rothman, S. (1984). Synaptic release of excitatory amino acid neuro-transmitter mediates anoxic neuronal death. J. Neurosci. 4, 1884–1891.
Benveniste, H., Drejer, J., Schousboe, A. and Diemer, N.H. (1984). Elevation of the extracellular concentrations of glutamate and aspartate in rat hippocampus during transient cerebral ischemia monitored by intracerebral microdialysis. J. Neurochem. 43, 1369–1374.
Simon, R.P., Swan, J.H. Griffiths, T. and Meldrum, B.S. (1984). Blockade of N-methyl-D-aspartate receptors may protect against ischemic damage in the brain. Science 226, 850–852.
Olney, J.W. (1979). Excitotoxic amino acids and Huntington’s disease. In Advances of Neurology, Huntington’s Disease, Vol. 23, Chase, T.N., Wexler, A. and Barbeau, A., eds., Raven, New York, pp. 609–624.
Beal, M.F., Kowall, N.W., Ellison, P.W., Mazurek, M.F., Swartz, K.J. and Martin, J.B. (1986). Replication of the neurochemical characteristic of Huntington’s disease by quinolinic acid. Nature 321(6066), 168–171.
Young, A.B., Greenmayre, J.T. and Penney, J.B. (1986). Glutamate receptors in Alzheimer’s disease. In Excitatory Amino Acid Transmission, Hicks, T.P., Lodge, D., McLennan, H., eds., Alan R. Liss, New York, pp. 233–240.
Olney, J.W. (1986). Inciting excitotoxic cytocide among central neurons. In Excitatory Amino Acids and Epilepsy, Schwarcz, R., Ben-Ari, Y., eds., Plenum, New York, pp. 631–646.
Olney, J.W., Price, M.T., Fuller, T.A., Labruyere, J., Samson, J., Carpenter, M. and Mahan, K. (1986). The anti-excitotoxic effects of certain anesthetics, analgesics and sedative-hypnotics. Neurosci. Lett. 68, 29–35.
Davies, J., Evans, R.H. and Jones, A.W. (1982). Differential activation and blockade of excitatory amino acid receptors in the mammalian and amphibian central nervous systems. Comp. Biochem. Physiol. 72, 211–224.
Rothman, S.M. (1985). The neurotoxicity of excitatory amino acids is produced by passive chloride influx. J. Neurosci. 5, 1483–1489.
Olney, J.W., Price, M.T., Samson, L. and Labruyere, J. (1986). The role of specific ions in glutamate neurotoxicity. Neurosci. Lett. 65, 65–71.
Mayer, M., Westbrook, G. and Forsythe, I. (1986). NMD A receptor function: Clues from biophysical experiments. In Excitatory Amino Acid Transmission, Hicks, T.P., Lodge, D. and McLennan, H., eds., Alan R. Liss, New York, pp. 27–34.
Anis, N.A., Berry, S.C., Burton, N.R. and Lodge, D. (1983). The dissociative anesthetics, ketamine and phencyclidine, selectively reduce excitation of central mammalian neurons by N-methyl-aspartate. Br. J. Pharmacol. 79, 565–575.
Choi, D.W. (1985). Two mechanisms underlying glutamate neurotoxicity in cortical cell culture. Neurosci, Abst. 11, 153.
Kim, J.S. (1983). Cerebral glutamate, neuroleptic drugs and schizophrenia: Increase of cerebrospinal fluid glutamate levels and decrease of striatal glutamate levels following sulpiride treatment in rats. Eur. Neurology 22, 367.
Simpson, G.M., Les, H., Branchey, M.H. and Shrivastavai, R.K. (1978). Boclofen in the treatment of tardive dyskinesia. Psychopharmacol. Bull. 14, 16–18.
Morris, R.G., Anderson, E., Lynch, G.S. and Baudry, M. (1986). Selective impairment of learning and blockade of long-term potentiation by an N-methyl-D-aspartate receptor antagonist, AP5. Nature 319(6056), 774–776.
Monoghan, D.T. and Cotman, C.W. (1985). Distribution of N-methyl-D-aspartate sensitive L-3H-glutamate-binding sites in rat brain. J. Neurosci. 5, 2909–2919.
Quang Do, Mattenberger, M., Streit, P. and Cuenod, M. (1986). In vitro release of endogenous excitatory sulfur-containing amino acids from various rat brain regions. J. Neurochem. 46, 779–786.
Olney, J.W., Price, M.T., Shahid Salles, K., Labruyere, J., Ryerson, R. and Mahan, K. (1986). L-homocysteic acid: A potent endogenous excitotoxin and putative transmitter. Neurosci. Abst. 12, 380.
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1988 Kluwer Academic Publishers
About this chapter
Cite this chapter
Olney, J.W. (1988). Excitatory Transmitters and Neuropsychiatry Disorders. In: Ferrendelli, J.A., Collins, R.C., Johnson, E.M. (eds) Neurobiology of Amino Acids, Peptides and Trophic Factors. Topics in the Neurosciences, vol 8. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1721-0_4
Download citation
DOI: https://doi.org/10.1007/978-1-4613-1721-0_4
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4612-8969-2
Online ISBN: 978-1-4613-1721-0
eBook Packages: Springer Book Archive