• Malin C Lagerström, Katarzyna Rogoz, Bjarke Abrahamsen, Emma Persson, Björn Reinius, Karin Nordenankar, Caroline Olund, Casey Smith, José Alfredo Mendez, Zhou-Feng Chen, John N Wood, Asa Wallén-Mackenzie, and Klas Kullander.
• Department of Neuroscience, Uppsala University, Box 593, 751 24 Uppsala, Sweden.
• Neuron. 2010 Nov 4;68(3):529-42.

AbstractThe 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.Copyright © 2010 Elsevier Inc. All rights reserved.

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