Scientists identify channel that protects against pain
Researchers from the University of Bristol identified an ion channel which limits spontaneous pain.
Scientists at the University of Bristol have identified a channel present in many pain-detecting neurones, which acts as a "brake" to limit spontaneous pain.
Spontaneous pain is defined as ongoing pathological pain which can be constant, slow burning pain, or intermittent, sharp shooting pain. It can be associated with many types of disease, damage or inflammation of tissues, nerves or organs.
The slow burning pain remains very difficult to treat effectively, according to the university, due to a lack of understanding of the mechanisms behind this type of pain.
Previously, research has found that spontaneous burning pain is due to constant activity in small sensory nerve fibers, known as C-fiber nociceptors, or pain neurons. While it is known that greater activity relates to greater pain, the causes and limits of this activity were, until now, poorly understood.
Bristol researchers have now uncovered an ion channel, known as TREK2, which is present exclusively in the membranes of these C-fiber neurons. According to the study, which has been published in the Journal of Neuroscience, TREK2 provides an natural protection against spontaneous pain.
Findings suggest that when TREK2 was removed from the proximity of the cell membrane, the membrane potentials become less negative, which translates into more firing, and therefore more pain. Membrane potentials also became more negative when the neuron was prevented from synthesising with TREK2.
Spontaneous pain associated with skin inflammation was found to increase when synthesis of TREK2 in C-fiber neurones was reduced.
Researchers concluded that in these C-fiber neurones, TREK2 stabilised membrane potential and decreased the likelihood of firing, thereby limiting the amount of spontaneous burning pain.
Professor Sally Lawson from the university's School of Physiology and Pharmacology, explained: "It became apparent that TREK2 was 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."
Lead author Dr Cristian Acosta, added: "We hope that this research will enable the development of methods to enhance the actions of TREK2, which could provide relief for sufferers of ongoing spontaneous burning pain in the future."
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