ST. LOUIS -- Nerve cells with a mutant calcium channel don't communicate as effectively as those with a normal calcium channel, according Saint Louis University research that is published in the Proceedings of the National Academy of Sciences Online Early Edition the week of Oct. 4.
"The research helps us understand the basic mechanism that underlies how neurons communicate," said Amy Harkins, Ph.D., assistant professor of pharmacological and physiological science at Saint Louis University School of Medicine and principal investigator.
"The entry of calcium into cells is a very important process that allows muscles to contract, the heart to beat and nerve cells to communicate with one another. The research is teaching us how a very integral part of our cellular structure works."
Communication between nerve cells occurs when calcium enters a nerve cell and causes the cell to release a chemical called a neurotransmitter that then carries a signal to other nerve cells. Calcium cannot freely enter cells, and must wait for an opening of a molecular gate, which is called a calcium channel.
"In this study we removed a specific part of the calcium channel molecule called the 'synaptic protein interaction site' and put this mutant calcium channel back into cells," Dr. Harkins said. "We found that cells with the mutant calcium channel no longer released neurotransmitter as efficiently as cells with the normal calcium channel."
The research, done in collaboration with investigators at The University of Chicago and Tufts University, is important in helping us understand more about the important process of communication between nerve cells, Dr. Harkins said.
"It gives us a basic understanding of how something works. In some ways, the body is similar to a broken car. When something goes wrong, you can't fix it if you don't know how it works."
The above post is reprinted from materials provided by Saint Louis University. Note: Materials may be edited for content and length.
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