皮膚在受傷、發(fā)炎或日灼后會(huì)變得高度敏感,，即便是最輕的碰觸也會(huì)引起強(qiáng)烈疼痛,。這種疼痛通常會(huì)很快消失，但在某些情況下它則會(huì)持久存在，造成難以治愈的,、讓人痛苦不堪的疼痛,，部分原因是其中所涉及的神經(jīng)回路的身份沒(méi)有確定。現(xiàn)在研究人員發(fā)現(xiàn),，新的一類(lèi)初級(jí)傳感神經(jīng)元與這些慢性疼痛綜合癥有關(guān),。
缺少非傳統(tǒng)“囊泡谷氨酸轉(zhuǎn)運(yùn)體” VGLUT3的突變小鼠，對(duì)強(qiáng)烈機(jī)械性疼痛敏感性降低,，對(duì)受傷之后的輕觸不再高度敏感,。背根神經(jīng)節(jié)中的VGLUT3+神經(jīng)元是無(wú)髓低閾限機(jī)械受體，它們被發(fā)現(xiàn)與人類(lèi)的愉快觸覺(jué)有關(guān),，而在受傷后的高度敏感期間它們傳遞的似乎是一種痛感,。這一發(fā)現(xiàn)為實(shí)驗(yàn)和治療干預(yù)提供了新途徑。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
