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Excitotoxicity and Neuropsychiatric Disorders

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Glutamate, Cell Death and Memory

Part of the book series: Research and Perspectives in Neurosciences ((NEUROSCIENCE))

Abstract

Three decades ago, Curtis and Watkins (1963), using newly developed micro-electrophoretic techniques to examine the membrane-depolarizing properties of glutamate (Glu) and related compounds, characterized the structural requirements for molecular interaction with an apparent excitatory amino acid (EAA) receptor. However, the myriad metabolic involvements of Glu, its ability to excite neurons throughout the central nervous system (CNS) and the lack of any known mechanism for terminating its excitatory action led neuroscientists of the 1960s and 1970s to reject Glu as a transmitter candidate. This view has yielded slowly to evidence that Glu satisfies the criteria for a transmitter and today this common acidic amino acid is widely accepted as the front-running transmitter candidate at the majority of excitatory synapses in the mammalian CNS.

Supported in part by NIMH Research Scientist Award MH 38894 (JWO) and HHS grants HD 24237, DA 05072 and AG 05681

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Olney, J.W. (1991). Excitotoxicity and Neuropsychiatric Disorders. In: Ascher, P., Choi, D.W., Christen, Y. (eds) Glutamate, Cell Death and Memory. Research and Perspectives in Neurosciences. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-84526-0_8

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