CHAPEL HILL Neurons, or nerve cells, communicate with each other through contact points called synapses. When these connections are damaged, communication breaks down, causing the messages that would normally help our feet push our bike pedals or our mind locate our car keys to fall short.
Now scientists at the University of North Carolina at Chapel Hill School of Medicine have shown that a protein called neurexin is required for these nerve cell connections to form and function correctly.
The discovery, made in Drosophila fruit flies may lead to advances in understanding autism spectrum disorders, as recently, human neurexins have been identified as a genetic risk factor for autism.
"This finding now gives us the opportunity to see what job neurexin performs within the cell, so that we can gain a better insight into what can go wrong in the nervous system when neurexin function is lost said Dr. Manzoor Bhat, associate professor of cell and molecular physiology in the UNC School of Medicine and senior author of the study.
The study, published online September 6, 2007, in the journal Neuron, is the first to successfully demonstrate in a Drosophila model the consequences that mutating this important protein may have on synapses.
The research was supported in part by grants from the National Institute of General Medical Sciences, National Institute of Neurological Disorders and Stroke and the National Institute of Mental Health and funds from the state of North Carolina.
During the last decade, scientists have learned that neurexins are integral to the transmission of chemical signals within the nervous system. Neurexins interact with binding partners called neuroligins to link neighboring nerve cells together so that signals can be sent and received correctly.
Previous attempts to study these proteins in animal models have been challenging. In vertebrates such as mice, three different genes code
|Contact: Les Lang|
University of North Carolina at Chapel Hill