Schizophrenia is a debilitating neurodevelopmental disorder affecting approximately 1% of the population and imposing a significant burden on society. One of the most replicated and well-established postmortem findings is a deficit in the expression of the gene encoding the 67-kDa isoform of glutamic acid decarboxylase (GAD67), the primary GABA-producing enzyme in the brain. GAD67 is expressed in various classes of interneurons, with vastly different morphological, molecular, and physiological properties. Importantly, GABA system deficits in schizophrenia encompass multiple interneuronal subtypes, raising several important questions. First, do different classes of interneurons regulate different aspects of behavior? Second, can we model cell-type-specific GABAergic deficits in mice, and will the rodent findings translate to human physiology? Finally, will this knowledge open the door to knowledge-based approaches to treat schizophrenia?
Copyright © 2012 S. Karger AG, Basel.