VGLUT2-dependent sensory neurons in the TRPV1 population regulate pain and itch.
VGLUT2-dependent sensory neurons in the TRPV1 population regulate pain and itch.
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DOI：
10.1016/j.neuron.2010.09.016
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发表时间：
2010-11-04
期刊：
影响因子：
16.2
通讯作者：
Kullander, Klas
中科院分区：
文献类型：
--
作者：
Lagerstrom, Malin C.;Rogoz, Katarzyna;Abrahamsen, Bjarke;Persson, Emma;Reinius, Bjorn;Nordenankar, Karin;Olund, Caroline;Smith, Casey;Mendez, Jose Alfredo;Chen, Zhou-Feng;Wood, John N.;Wallen-Mackenzie, Asa;Kullander, Klas
对痒感的自然反应是抓挠，通过一种未知的机制来缓解痒。疼痛和瘙痒之间的相互作用经常被证明，基于电生理和行为实验的数据，瘙痒的选择性假设假设存在能够抑制瘙痒的初级疼痛传入。在这里，我们证明了在与香草受体（TRPV1）初级传入神经部分重叠的神经元亚群中，水泡状谷氨酸转运蛋白（VGLUT） 2的缺失导致瘙痒行为急剧增加，同时对热痛的反应性降低。通过抗组胺药和胃泌素释放肽受体的基因缺失，增加的瘙痒行为减少，表明VGLUT2依赖于维持组胺能和非组胺能瘙痒的正常水平。本研究证实VGLUT2在TRPV1热痛觉中起主要作用，并调节正常的瘙痒反应。
The natural response to itch sensation is to scratch, which relieves the itch through an unknown mechanism. Interaction between pain and itch has been frequently demonstrated, and the selectivity hypothesis of itch, based on data from electrophysiological and behavioral experiments, postulates the existence of primary pain afferents capable of repressing itch. Here, we demonstrate that deletion of vesicular glutamate transporter (VGLUT) 2 in a subpopulation of neurons partly overlapping with the vanilloid receptor (TRPV1) primary afferents resulted in a dramatic increase in itch behavior accompanied by a reduced responsiveness to thermal pain. The increased itch behavior was reduced by administration of antihistaminergic drugs and by genetic deletion of the gastrin-releasing peptide receptor, demonstrating a dependence on VGLUT2 to maintain normal levels of both histaminergic and nonhistaminergic itch. This study establishes that VGLUT2 is a major player in TRPV1 thermal nociception and also serves to regulate a normal itch response.
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