The Impact of Oxidative Stress on GAD67 Levels and Parvalbumin-Positive Neurons

摘要: GAD67, product of the GAD1 gene, and GAD65, GAD2, are critically involved in control GABA synthesis central nervous system. Since initial report decreased transcription levels GAD67 prefrontal cortex patients with schizophrenia, finding GAD transcript protein has been very generally replicated, making it most consistent neurochemical abnormality schizophrenia to some extent bipolar affective disorder. The concomitant decrease calcium-binding parvalbumin reported similar regularity, these perturbations relate dysfunction a network cortical or hippocampal GABAergic interneurons, notably basket chandelier cells. Among potential mechanisms leading this decrease, hypofunction NMDA receptor attracted attention shown recently involve increased oxidative stress, originating from NADPH oxidase activation. Lastly, large preclinical cognitive literature suggests that dysfunctional frontal is associated abnormal electroencephalographic spectra, which thought underlie higher functions known be disturbed schizophrenia.