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Titlebook: Excitotoxins; Proceedings of an In Kjell Fuxe,Peter Roberts,Robert Schwarcz Conference proceedings 1983 Springer Science+Business Media New

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Electrophysiological Actions of Kainate and Other Excitatory Amino Acids, and the Structure of Theirlarize and excite neurones of the mammalian spinal cord (Curtis, .., 1959; 1960), and that similar excitatory effects could be elicited by a variety of other compounds chemically related to the natural substances (Curtis and Watkins, 1960; 1963). Curtis and Watkins (1960) set forth the criteria whic
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Recent Advances in the Pharmacology of Excitatory Amino Acids in the Mammalian Central Nervous Systeagonists and antagonists for NMA receptors and non-NMA receptors are summarized. New NMA receptor antagonists include a range of D-aspartyl- and D-glutamyl dipeptides where the second amino acid contains a phosphonic acid moiety. None of these dipeptides is more potent or specific than 2-amino-5-pho
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Alteration by Kainate of Energy Stores and Neuronal-Glial Metabolism of Glutamate ,amate and aspartate from the tissue and decreased the synthesis of glutamine from a variety of radioactive precursors. These effects were attributed to alterations in glial cells secondary to massive depolarization of neurons. These results and those of others are discussed in terms of their implica
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Excitotoxins: An Overviewfor the effort spent in pursuing these challenges. If we are right in suspecting that endogenous excitotoxins--glutamate (Glu), aspartate (Asp) and perhaps others--are the neurotransmitters released at the majority of excitatory synapses in the mammalian CNS, this is reason enough for our intrigue w
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Kainic Acid: Insights into Its Receptor-Mediated Neurotoxic Mechanismsrmationally restricted analogue of L-glutamate, it was a potent agonist at glutamate receptors (Olney .., 1974; Coyle and Schwarcz, 1976). Since the first reports of the perikaryal-specific neurotoxic action of intracerebrally injected KA, it has become increasingly apparent that the mechanism of it
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The Neurodegenerative Properties of Intracerebral Quinolinic Acid and its Structural Analog Cis-2,3- have led to the hypothesis that human neurodegenerative diseases, e.g. Huntington’s disease (HD) and temporal lobe epilepsy, may be related to a pathological overproduction of endogenous neuroexcitatory amino acids (Coyle et al., 1977; Divac, 1977; Olney and de Gubareff, 1978; French et al., 1982).
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