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- W128251254 endingPage "195" @default.
- W128251254 startingPage "181" @default.
- W128251254 abstract "The glutamate (GLU) hypothesis of schizophrenia was first published in 1980 and was based on reduced Glu levels in the cerebrospinal fluid (CSF) of schizophrenic patients (1). Although it took a while, this negative correlation between Glu levels and schizophrenic symptoms has recently been confirmed (2). Further evidences are also in concert with a hypoactive glutamatergic system as one but not solely underlying mechanism in schizophrenia (see Chapter 7 by Bleich and Kornhuber) and one of these major findings is going back to the late 1950s when schizophrenia-like symptoms were described after administration of phencyclidine (PCP) in humans (3). However, a link between PCP-induced effects and the glutamatergic system was drawn not earlier than 20 years later when an interaction of PCP with the GluR and more specifically with the N-methyl-d-aspartate (NMDA) receptor was shown (4–6). Further antagonists that block the NMDA receptor in a competitive or noncompetitive manner induce schizophrenialike symptoms as well when they are given to humans and also to animals (7–11). More support for the GLU hypothesis derived from postmortem studies showing an increase of NMDA receptor density in several brain areas (12–13) most probable as a consequence of lowered GLU release in these regions although differences regarding the NMDA subunits can be seen (14–15). Adaptation in the density of other GluRs as α-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA), kainate-, and metabotropic receptors has also been described, but the findings are less concise and depend on the respective subunit of the receptor and on the anatomical structures (14,16–17)." @default.
- W128251254 created "2016-06-24" @default.
- W128251254 creator A5018664066 @default.
- W128251254 date "2005-01-01" @default.
- W128251254 modified "2023-09-23" @default.
- W128251254 title "Role of Glycine in Schizophrenia" @default.
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