Dysfunction of Glia-Neuron Communication in Pathophysiology of Schizophrenia
Multiple lines of evidence suggest that genetic factors and environmental factors as well as a dysfunction in the glutamatergic neurotransmission contribute to the pathophysiology of schizophrenia. Communication between neurons and glia is essential for axonal conduction, synaptic neurotransmission, and information processing, and thus is required for normal functioning of the nervous system during development and throughout adult life. A number of studies have demonstrated that the substances which communicate between neurons and glia are altered in the blood, cerebrospinal fluid (CSF), and postmortem brain samples of schizophrenic patients. These findings suggest that neuron-glia communication might be impaired in the brains of schizophrenic patients. In this article, we review the imbalance of neuron-glia communication presented in the neurodevelopmental hypothesis as well as the glutamate hypothesis of schizophrenia. First, we discuss the role of growth factors (e.g., basic fibroblast growth factor (bFGF), epidermal growth factor (EGF), midkine), brain-derived neurotrophic factor (BDNF) and cytokines in the pathophysiology of schizophrenia. Second, we focus on the role of endogenous substances (glutamate, glutamine, D-serine, kynurenic acid, and glutathione), which modulate the NMDA receptor function, in the pathophysiology of schizophrenia.
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Document Type: Review Article
Affiliations: Department of Psychiatry, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chiba 260- 8670, Japan.
Publication date: June 1, 2005
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