A recent study on pain sensation opines that a certain set of nerve fibers may be responsible for making injured areas overly sensitive to touch. Results of the study were arrived at by studying such reactions in mice.
When a person has any kind of injury - a broken shin, for example a sunburn - the pain system becomes hypersensitive, firing up in response to normally painless sensations induced by, for instance, walking or a gentle massage.
While normally, this tenderness protects the vulnerable tissue as it heals, occasionally, the pain can overstay becoming chronic in conditions such as arthritis.
Now, neuroscientists Robert Edwards and Allan Basbaum from the University of California, San Francisco, and their colleagues have found that a small subset of nerve fibers could be routing innocuous touch sensations to a once-mysterious neural pathway when there's an injury.
"Surprise would be an understatement. No one knew anything about what these fibers were doing," Nature quoted Basbaum as saying.
The researchers found that the fibers, called unmyelinated low-threshold mechanoreceptors (C-LTMRs), are easily stimulated, unlike classic pain fibers, which respond only when the sensation is intense.
But C-LTMRs aren't usually used to detect light touch - this falls to another major group of sensory neurons - so their role was unclear.
The researchers then discovered that these fibers express VGLUT3, a protein necessary for the cells to send signals to other neurons.
Because all of the other sensory neurons going to the spinal cord use a different protein - VGLUT1 or VGLUT2 - the authors could engineer mice lacking VGLUT3 to render all of the C-LTMRs silent.
Mice without functional C-LTMRs responded in exactly the same way as normal mice when exposed to light touch and to most painful stimuli, including extreme cold or heat or being poked in the paw with thin wires.
But then the authors tested how the mice responded after being injured in three other ways: by a chemical that causes inflammation, which occurs in situations ranging from muscle injuries to a misaligned back; an incision, mimicking pain after surgery; and nerve damage.
In all three types of injury, normal mice became much more sensitive to wires poking their paws, quickly flicking the wires away.
But mice with silent C-LTMRs showed much the same responses as before they were injured.
All mice, however, became more sensitive to heat, suggesting that the C-LTMRs were hyposensitizing the animals to touch rather than to temperature.
"The data shows that recruitment of these fibers is a new way of producing mechanical hypersensitivity. It's an exciting example of the specific functions of different sets of sensory neurons," says neuroscientist Clifford Woolf at Harvard Medical School in Boston, Massachusetts.
The team's findings are published in Nature.