Recent studies have identified many genes that may put people at risk for schizophrenia. But what links genetic differences to changes in altered brain activity in schizophrenia is not clear. Now, three laboratories at the Perelman School of Medicine at the University of Pennsylvania have come together, using electrophysiological, anatomical, and immunohistochemical approaches - along with a unique high-speed imaging technique - to understand how schizophrenia works at the cellular level, especially in identifying how changes in the interaction between different types of nerve cells lead to symptoms of the disease. The findings were reported online on October 3, 2011 in the Proceedings of the National Academy of Sciences. "Our work provides a model linking genetic risk factors for schizophrenia to a functional disruption in how the brain responds to sound, by identifying reduced activity in special nerve cells that are designed to make other cells in the brain work together at a very fast pace," explains lead author Dr. Gregory Carlson, assistant professor of Neuroscience in Psychiatry. "We know that in schizophrenia this ability is reduced, and now, knowing more about why this happens may help explain how loss of a protein called dysbindin leads to some symptoms of schizophrenia." Previous genetic studies had found that some different forms of the gene for dysbindin were found in people with schizophrenia. Most importantly, a prior finding at Penn showed that the dysbindin protein is reduced in a majority of schizophrenia patients, suggesting it is involved in a common cause of the disease. For the current PNAS study, Dr. Carlson, Dr. Steven J. Siegel, associate professor of Psychiatry, director of the Translational Neuroscience Program; and Dr. Steven E.
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