The kinin B1 receptor mediates alloknesis in a murine model of inflammation

Neuroscience Letters
Jumian FengWenjin Ji

Abstract

Noxious stimuli and non-noxious mechanical stimuli elicit itch (alloknesis) instead of pain on skin lesions of patients with atopic dermatitis. We previously found that bradykinin evokes an itch-related scratching response through activation of kinin B1 receptor in skin inflamed using complete Freund's adjuvant. In this study we investigated whether alloknesis is evoked in CFA-inflamed skin and the involvement of kinin receptors. In our results, alloknesis was elicited four days after CFA-inflammation. Furthermore, pretreatment with a B1 receptor antagonist or μ-opioid receptor antagonist significantly reduced alloknesis. In contrast, treatment with a B2 receptor antagonist significantly increased alloknesis. These results suggest that the alloknesis response is mediated by the activation of kinin B1 receptor but antagonized by the B2 receptor in CFA-inflamed mice.

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Citations

Nov 10, 2015·Peptides·Richard J Bodnar
Nov 25, 2014·Naunyn-Schmiedeberg's Archives of Pharmacology·Xuming Zhang
Jul 26, 2017·Molecular Pain·Stacie K Totsch, Robert Ernest Sorge
Nov 24, 2017·Expert Opinion on Therapeutic Targets·Fatimunnisa Qadri, Michael Bader
Sep 25, 2017·American Journal of Physiology. Lung Cellular and Molecular Physiology·Chhinder P SodhiHongpeng Jia
Jul 26, 2016·Experimental and Therapeutic Medicine·Yuanzhen ChenWenjin Ji

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