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.
Source-ANI
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