Injury-induced mechanical hypersensitivity requires C-low threshold mechanoreceptors

Rebecca P. Seal, Xidao Wang, Yun Guan, Srinivasa N. Raja, C. Jeffery Woodbury, Allan I. Basbaum and Robert H. Edwards ()
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Rebecca P. Seal: University of California, San Francisco School of Medicine, California 94143, USA
Xidao Wang: University of California, San Francisco School of Medicine, California 94158, USA
Yun Guan: the Johns Hopkins University, School of Medicine, Baltimore, Maryland 21205, USA
Srinivasa N. Raja: the Johns Hopkins University, School of Medicine, Baltimore, Maryland 21205, USA
C. Jeffery Woodbury: University of Wyoming, Laramie, Wyoming 82071, USA
Allan I. Basbaum: University of California, San Francisco School of Medicine, California 94158, USA
Robert H. Edwards: University of California, San Francisco School of Medicine, California 94143, USA

Nature, 2009, vol. 462, issue 7273, 651-655

Abstract: A touch painful The skin can become hypersensitive following injury, inflammation or sunburn, when even the lightest touch can cause intense pain. This usually disappears quickly, but in some cases it persists, causing debilitating pain that is hard to treat, in part because the identity of the neural circuits involved is not known. Now a novel class of primary sensory neurons has been implicated in these chronic pain syndromes. Mutant mice lacking the unconventional vesicular glutamate transporter VGLUT3 become less sensitive to intense mechanical pain and are no longer hypersensitive to light touch after injury. The VGLUT3+ neurons in the dorsal root ganglion are unmyelinated low-threshold mechanoreceptors that have been implicated in pleasant touch sensations in humans, and it appears that during post-injury hypersensitivity they instead convey a sensation of pain. This suggests new avenues for experiment and therapeutic intervention.

Date: 2009
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DOI: 10.1038/nature08505

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