Channel that acts like brake against pain identified

Scientists have identified a channel present in many pain detecting sensory neurons that acts as a 'brake', limiting spontaneous pain.

Research from the University of Bristol, has identified a particular ion channel present exclusively in these C-fiber nociceptors.

This ion channel, known as TREK2, is present in the membranes of these neurons, and the researchers showed that it provides a natural innate protection against this pain.

Ion channels are specialised proteins that are selectively permeable to particular ions. They form pores through the neuronal membrane.

Leak potassium channels are unusual, in that they are open most of the time allowing positive potassium ions (K+) to leak out of the cell.

This K+ leakage is the main cause of the negative membrane potentials in all neurons. TREK2 is one of these leak potassium channels. Importantly, the C-nociceptors that express TREK2 have much more negative membrane potentials than those that do not.

Researchers showed that when TREK2 was removed from the proximity of the cell membrane, the potential in those neurons became less negative. In addition, when the neuron was prevented from synthesizing the TREK2, the membrane potential also became less negative.

They also found that spontaneous pain associated with skin inflammation, was increased by reducing the levels of synthesis of TREK2 in these C-fiber neurons.

They concluded that in these C-fiber nociceptors the TREK2 keeps membrane potentials more negative, stabilizing their membrane potential, reducing firing and thus limiting the amount of spontaneous burning pain.

The research has been published in the Journal of Neuroscience.