Potential New Target for Managing Spontaneous Burning Pain


Researchers have identified a component of particular nociceptors associated with neuropathic pain that may act to naturally limit the severity of pain.

Researchers from the School of Physiology and Pharmacology at Bristol University in the United Kingdom have identified an ion channel found only in the membranes of C-fiber nociceptors, which are the neurons are associated with neuropathic pain.

They suggested that the channel may act as a “brake” and protect against spontaneous pain. The results from their study were published in The Journal of Neuroscience.

This ion channel (TREK2) is an example of what are known as “leak potassium channels,” which allow positive potassium ions (K+) to leak out of the cell, causing negative membrane potential.

According to a news release that accompanied publication of the study results, the researchers found that removing TREK2 from the proximity of the cell membrane of these neurons or altering the cells so they do not synthesize TREK2 makes their cell membranes much less negative. They also found that the nociceptors that express TREK2 have "much more negative membrane potentials than those that do not.”

They reported that reduced levels of TREK2 synthesis were linked to increased spontaneous pain associated with skin inflammation. They concluded that in these particular nociceptors, TREK2 “keeps membrane potentials more negative, stabilizing their membrane potential, reducing firing and thus limiting the amount of spontaneous burning pain.”

During the study, “it became evident that TREK2 kept the C-fiber nociceptor membrane at a more negative potential,” said Sally Lawson, BSc, Phd, from the School of Physiology and Pharmacology at Bristol University.

These results demonstrate that TREK2 in C-fiber nociceptors “is important for stabilizing their membrane potential and decreasing the likelihood of firing. It became apparent that TREK2 was thus likely to act as a natural innate protection against pain. Our data supported this, indicating that in chronic pain states, TREK2 is acting as a brake on the level of spontaneous pain,” said Lawson.

Lead author Cristian Acosta, PhD, said “Given the role of TREK2 in protecting against spontaneous pain, it is important to advance our understanding of the regulatory mechanisms controlling its expression and trafficking in these C-fiber nociceptors. We hope that this research will enable development of methods of enhancing the actions of TREK2 that could potentially some years hence provide relief for sufferers of ongoing spontaneous burning pain.”

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