Alcohol withdrawal is often associated with severe headache, which contributes to the ongoing struggle of the roughly 283 million people worldwide suffering from alcohol use disorder. Severe headache often pushes rehabilitating patients back to alcohol, because they know that drinking will reduce the headache, but unfortunately it is a vicious cycle.
Researchers at The University of Texas Health Science Center at San Antonio have identified a critical link that connects a stress hormone and immune cells to these alcohol withdrawal headaches. Their study, published in Neuron, highlights the central role of the stress hormone, corticotropin-releasing factor (CRF), which triggers the activation of mast cells located in the dura, a thin membrane beneath the skull.
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The dura contains peripheral nerve fibers and peripheral blood vessels. When CRF binds to a specific mast cell receptor called MrgprB2, it sets off a chain reaction that leads to various functions, including blood vessel dilation. This process activates sensory neurons, resulting in a heightened sensitivity that manifests as an alcohol withdrawal headache.
This discovery paves the way for further research into substance use disorder mechanisms, particularly withdrawal. It holds the potential for the development of small-molecule drug therapies that can inhibit the interaction between CRF and MrgprB2, potentially reducing the pain signals associated with alcohol withdrawal and offering hope for improved treatments.