![Scientists at the University of Bristol have discovered an ion channel that protects against spontaneous pain. Spontaneous pain is ongoing pathological pain that lacks an […]](/wp-content/uploads/2013/02/NEWSICON2-620x300.png "Ion Channel Protects Against Pain")
Scientists at the University of Bristol have discovered an ion channel that protects against spontaneous pain. Spontaneous pain is ongoing pathological pain that lacks an immediate trigger and results from the spontaneous firing of neurons that carry pain signals from the site of injury to the spinal cord (C-fibre nociceptors). Additional neurons then carry information about the pain stimulus from the spinal cord to the brain, where the pain perception is generated. The research published last week in the Journal of Neuroscience provides a window of opportunity for new ways to treat chronic pain.
The ion channel, TREK2 is present in C-fibre nociceptors, and allows potassium ions (K+) to flow out of the neurons. The outflow of these positively charged ions means that the neuron is less likely to become excited and fire an action potential. Disruption of pain signal relay via the spinal cord to the brain reduces the amplitude of the pain percept.
The research group used a mouse model to demonstrate that TREK2 channels reduce spontaneous pathological pain. Mice with TREK2 gene knockdown (fewer TREK2 channels) showed increased foot lifting in response to a painful stimulus than control mice, indicating heightened pain perception (increased sensitivity). This supported the role of TREK2 channels in diminishing pain in vivo.
Future research is needed to clarify the mechanisms controlling TREK2 channel expression in C-fibre nocicieptors. By altering these mechanisms to increase the numbers of TREK2 channels in humans C-fibre nociceptors, we could potentially generate a new way of reducing chronic pain without the need for pain-relieving drugs.
Read more at: http://www.jneurosci.org/content/34/4/1494.short?rss=1
