Abstract
Growing evidence suggests an involvement of excitatory amino acid (EAA) systems in schizophrenia. Precedent exists for changes in binding to kainate, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, N-methyl-D-aspartate subtypes of EAA receptors. Current evidence indicates that in schizophrenia, EAA receptor levels can be decreased, unchanged, or even increased in certain brain regions and certain cases. It is likely that variability may arise from different drug histories of patients, other coexistent and undetected disease states, and the inherent heterogeneity of schizophrenia. On the other hand, it is possible that schizophrenia reflects a pattern of imbalances, not a simple unidirectional change. If so, even subtle changes may contribute significantly to the overall status of ongoing circuitry function in key brain areas implicated in schizophrenia. Together with other neurotransmitter systems, for example, dopaminergic, the net effect of EAA receptor imbalances may be greater than changes in the individual receptors and their neurotransmitters.
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