ANN ARBOR, Mich. Researchers at the University of Michigan Health System have found a key linkage between pain and a specific brain molecule, a discovery that lends new insight into fibromyalgia, an often-baffling chronic pain condition.
In patients with fibromyalgia, researchers found, pain decreased when levels of the brain molecule called glutamate went down. The results of this study, which appears in the journal Arthritis and Rheumatism, could be useful to researchers looking for new drugs that treat fibromyalgia, the authors say.
If these findings are replicated, investigators performing clinical treatment trials in fibromyalgia could potentially use glutamate as a surrogate marker of disease response, says lead author Richard E. Harris, Ph.D., research assistant professor in the Division of Rheumatology at the U-M Medical School's Department of Internal Medicine and a researcher at the U-M Chronic Pain and Fatigue Research Center.
The molecule glutamate is a neurotransmitter, which means it conveys information between neurons in the nervous system. When glutamate is released from one neuron, it diffuses across the space between cells, and then binds to receptors on the next neuron in line and causes the cell to become excited, or to be more active.
This molecule was suspected to play a role in fibromyalgia because previous studies had shown that some brain regions in fibromyalgia patients appear to be highly excited. One such region is the insula.
In functional magnetic resonance imaging (fMRI) studies, researchers at U-M had previously shown that the insula displays augmented activity in fibromyalgia, which means neurons in these patients are more active in this part of the brain. The U-M team hypothesized, Harris notes, that more activity among these neurons might be related to the level of glutamate in this region.
To gauge the linkage between pain and glutamate, the researchers used a non-inva
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University of Michigan Health System