Abstract
A number of studies have suggested that disturbance in glutamatergic transmission in the cerebral cortex may underlie, or contribute to the pathophysiology of schizophrenia. In this study we examined expression of the postsynaptic density protein 95 (PSD95) mRNA in the prefrontal cortex and hippocampus in postmortem material from neuroleptic-treated schizophrenics and normal controls. PSD95 is known to bind to NMDA receptor subunits and is known to be involved in synaptic plasticity. In situ hybridization analysis showed that the expression of PSD95 was significantly decreased in Brodmann area 9 of the prefrontal cortex but not in the hippocampus. These results further implicate the prefrontal cortex in the pathophysiology of schizophrenia and suggest dysfunction of NMDA receptors in the schizophrenic cortex.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Aged
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Cerebellum / metabolism
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Cerebellum / pathology
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Cerebellum / physiopathology
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Disks Large Homolog 4 Protein
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Female
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Gene Expression Regulation / physiology
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Glutamic Acid / metabolism*
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Hippocampus / metabolism*
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Hippocampus / pathology
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Hippocampus / physiopathology
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Humans
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Intracellular Signaling Peptides and Proteins
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Male
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Membrane Proteins
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Middle Aged
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Nerve Tissue Proteins / genetics*
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Neuronal Plasticity / physiology
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Neurons / cytology
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Neurons / metabolism
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Prefrontal Cortex / metabolism*
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Prefrontal Cortex / pathology
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Prefrontal Cortex / physiopathology
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RNA, Messenger / metabolism
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Receptors, N-Methyl-D-Aspartate / metabolism*
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Schizophrenia / genetics*
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Schizophrenia / metabolism
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Schizophrenia / physiopathology
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Synaptic Membranes / metabolism
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Synaptic Transmission / physiology
Substances
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DLG4 protein, human
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Disks Large Homolog 4 Protein
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Intracellular Signaling Peptides and Proteins
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Membrane Proteins
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Nerve Tissue Proteins
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RNA, Messenger
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Receptors, N-Methyl-D-Aspartate
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postsynaptic density proteins
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Glutamic Acid