Dystroglycan Critical for Nervous System Development

Using a genetically engineered line of mice lacking the gene for dystroglycan, investigators from the University of Iowa (Iowa City, USA) found that the specific mutation they had introduced caused progressive nerve damage in the mice. The mice were less coordinated than normal mice, and their sensitivity to heat and pressure was altered. Moreover, nerve impulses traveled more slowly in these mice. At the molecular level, loss of dystroglycan reduced the density of the sodium channels that are critical for normal transmission of nerve impulses. These findings were published in the June 5, 2003, issue of Neuron.

"The slowing in the time it takes for a signal to travel along the nerve is really interesting,” said senior author Dr. Kevin Campbell, professor and interim head of physiology and biophysics and professor of neurology at the University of Iowa. "We think that dystroglycan may play a role in organizing the sodium channels at the nodes and setting up the proper nodal structure for efficient transmission of nerve signals.”




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