期刊
NEURON
卷 68, 期 3, 页码 529-542出版社
CELL PRESS
DOI: 10.1016/j.neuron.2010.09.016
关键词
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资金
- Swedish Medical Research Council [2003-2258, 2004-5567, 2007-3630/4479]
- Swedish Brain Foundation
- Foundations of Knut and Alice Wallenberg
- A. Wiberg
- M. Bergwall
- Ahlen
- Hedlund
- Uppsala University
- Knut and Alice Wallenberg Foundation
- BBSRC [BB/F000227/1] Funding Source: UKRI
- MRC [G0901905] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/F000227/1] Funding Source: researchfish
- Medical Research Council [G0901905] Funding Source: researchfish
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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