Titlebook: Glutamate, Cell Death and Memory; Philippe Ascher,Dennis W. Choi,Yves Christen Conference proceedings 1991 Springer-Verlag Berlin Heidelbe

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Blockade of Specific K+ Channels Produces a Ca++ Dependent Form of Long-Term Potentiation in the Hiic transmission, which is considered to be a good experimental model of memory processes (Teyler and DiScenna 1987). The mechanisms of the induction and maintenance phases of LTP have been extensively studied in this structure, which plays an important role in memory processes, and the injury of whi

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Excitotoxicity and Neuropsychiatric Disorders,f 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 lac

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In Vitro Neuronal Death: Contrasts Between Excitotoxicity and Chemical Hypoxia,s were extremely vulnerable to inhibition of oxidative metabolism. When cultures at least two weeks . were exposed to sodium cyanide or an atmosphere of 95% nitrogen/5% CO2, neurons swelled and eventually died (Rothman 1983). However, cultures exposed to similar insults one or two days after plating

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