皮肤在受伤、发炎或日灼后会变得高度敏感，即便是最轻的碰触也会引起强烈疼痛。这种疼痛通常会很快消失，但在某些情况下它则会持久存在，造成难以治愈的、让人痛苦不堪的疼痛，部分原因是其中所涉及的神经回路的身份没有确定。现在研究人员发现，新的一类初级传感神经元与这些慢性疼痛综合症有关。
缺少非传统“囊泡谷氨酸转运体” VGLUT3的突变小鼠，对强烈机械性疼痛敏感性降低，对受伤之后的轻触不再高度敏感。背根神经节中的VGLUT3+神经元是无髓低阈限机械受体，它们被发现与人类的愉快触觉有关，而在受伤后的高度敏感期间它们传递的似乎是一种痛感。这一发现为实验和治疗干预提供了新途径。（生物谷Bioon.com）
生物谷推荐原始出处：
Nature 462, 651-655 (3 December 2009) | doi:10.1038/nature08505
Injury-induced mechanical hypersensitivity requires C-low threshold mechanoreceptors
Rebecca P. Seal1,5, Xidao Wang2,5, Yun Guan3, Srinivasa N. Raja3, C. Jeffery Woodbury4, Allan I. Basbaum2 & Robert H. Edwards1
1 Departments of Physiology and Neurology, University of California, San Francisco School of Medicine, California 94143, USA
2 Departments of Anatomy and Physiology, University of California, San Francisco School of Medicine, California 94158, USA
3 Department of Anesthesiology and Critical Care Medicine, the Johns Hopkins University, School of Medicine, Baltimore, Maryland 21205, USA
4 Department of Zoology and Physiology, University of Wyoming, Laramie, Wyoming 82071, USA
5 These authors contributed equally to the work.
6 Correspondence to: Robert H. Edwards1 Correspondence and requests for materials should be addressed to R.H.E.
Mechanical pain contributes to the morbidity associated with inflammation and trauma, but primary sensory neurons that convey the sensation of acute and persistent mechanical pain have not been identified. Dorsal root ganglion (DRG) neurons transmit sensory information to the spinal cord using the excitatory transmitter glutamate1, a process that depends on glutamate transport into synaptic vesicles for regulated exocytotic release. Here we report that a small subset of cells in the DRG expresses the low abundance vesicular glutamate transporter VGLUT3 (also known as SLC17A8). In the dorsal horn of the spinal cord, these afferents project to lamina I and the innermost layer of lamina II, which has previously been implicated in persistent pain caused by injury2. Because the different VGLUT isoforms generally have a non-redundant pattern of expression3, we used Vglut3 knockout mice to assess the role of VGLUT3+ primary afferents in the behavioural response to somatosensory input. The loss of VGLUT3 specifically impairs mechanical pain sensation, and in particular the mechanical hypersensitivity to normally innocuous stimuli that accompanies inflammation, nerve injury and trauma. Direct recording from VGLUT3+ neurons in the DRG further identifies them as a poorly understood population of unmyelinated, low threshold mechanoreceptors (C-LTMRs)4, 5. The analysis of Vglut3 -/- mice now indicates a critical role for C-LTMRs in the mechanical hypersensitivity caused by injury.
