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What is Serotonin's Role in Chronic Pain?

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Written by Adam Zewe

Scientists at the University of Maryland School of Dentistry (UMSOD), in collaboration with colleagues from the Johns Hopkins University School of Medicine, have conducted innovative research that shows how mechanisms in the central nervous system can contribute to chronic pain after nerve injury. The January edition of the journal Neuron published their results: "Central Terminal Sensitization of TRPV1 by Descending Serotonergic Facilitation Modulates Chronic Pain."

The research seeks to explain what causes a patient to suffer from a condition called secondary hyperalgesia. In secondary hyperalgesia, a patient will experience hypersensitivity to pain in areas of the body that are near an injury. This pain can persist for months or years after the original injury has healed. For example, when a patient suffers from a toothache, he or she often feels pain on the entire side of the face, rather than only in the tooth that has been damaged. "We believe that secondary hyperalgesia is caused by central changes in the brain because there is no peripheral nerve injury. However, we had little evidence to support this theory," explains Feng Wei, MD, PhD, associate professor in the Department of Neural and Pain Sciences.

Wei and his collaborators developed a novel facial pain model to examine secondary hyperalgesia. They combined advanced genetic imaging with electrophysiological recordings to study activity in primary sensory neurons. They focused on the trigeminal nerve, which is responsible for sensation and motor functions in the face. The researchers examined the activity in the neurons' central terminals, which are the connections between the sensory neurons and the central nervous system. This is the first time this type of genetic imaging on the central terminals was used to study pain, Wei says.

The researchers were able to precisely study the neuronal hyper-excitability that occurs after a nerve injury. They determined that, when the molecule serotonin is released from the brain stem, it can activate serotonin receptors and cause hyper-excitability, which contributes to the persistence of chronic pain.

The development of this scientific model provides huge potential for future research on the cause of widespread chronic pain after nerve injury. Wei and his colleagues plan to study the individual subtypes of serotonin receptors to determine which are involved in pain caused by nerve injury. "If we could find a way to selectively target specific subtypes of serotonin receptors in central terminals of primary sensory neurons, then we could potentially develop a drug that prevents this type of chronic pain from occurring," says Wei.

Professors Ronald Dubner, DDS, PhD, and Ke Ren, PhD, MD, in the Department of Neural and Pain Sciences were also involved in the study. A research group led by Associate Professor Xinzhong Dong, PhD, in the Department of Neuroscience at Johns Hopkins School of Medicine contributed to this work.


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