title: Schizophrenia: from dopaminergic to glutamatergic interventions.
abstract: Schizophrenia might be considered a neurodevelopmental disease. However, the fundamental process(es) associated with this disease remain(s) uncertain. Many lines of evidence suggest that schizophrenia is associated with excessive stimulation of dopamine D2 receptors in the associative striatum, with a lack of stimulation of dopamine D1 receptors in prefrontal cortex, and with modifications in prefrontal neuronal connectivity involving glutamate transmission at N-methyl aspartate (NMDA) receptors. This article, whilst briefly discussing the current knowledge of the disease, mainly concentrates on the NMDA hypofunction hypothesis. However, there are also potential consequences for a Dopamine imbalance on NMDA function. Thus, it is proposed that schizophrenia has a complex aetiology associated with strongly interconnected aberrations of dopamine and glutamate transmission.
authors: New Medicines Neurosciences Therapeutic Area Head, UCB Pharma, S.A., Belgium. Electronic address: ml393@columbia.edu.
authors: Marc
authors: M
authors: Laruelle
mesh_terms: D000818:Animals; D003342:Corpus Striatum / Q000378:metabolism; D004298:Dopamine / Q000378:metabolism*; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D017397:Prefrontal Cortex / Q000378:metabolism; D017447:Receptors, Dopamine D1 / Q000378:metabolism; D017448:Receptors, Dopamine D2 / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism*; D012559:Schizophrenia / Q000188:drug therapy / Q000503:physiopathology*
chemical_list: D017447:Receptors, Dopamine D1; D017448:Receptors, Dopamine D2; D016194:Receptors, N-Methyl-D-Aspartate; D018698:Glutamic Acid; D004298:Dopamine