Expression of leukotriene receptors in the rat dorsal root ganglion and the effects on pain behaviorsReportar como inadecuado




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Molecular Pain

, 6:57

First Online: 17 September 2010Received: 21 June 2010Accepted: 17 September 2010

Abstract

BackgroundLeukotrienes LTs belong to the large family of lipid mediators implicated in various inflammatory conditions such as asthma and rheumatoid arthritis. Four distinct types BLT1, BLT2, CysLT1 and CysLT2 of G-protein-coupled receptors for LTs have been identified. Several studies have reported that LTs are involved in inflammatory pain, but the mechanism and the expression of LT receptors in the nociceptive pathway are unknown.

ResultsWe investigated the precise expression of these four types of LT receptors in the adult rat dorsal root ganglion DRG using reverse transcription-polymerase reaction RT-PCR and radioisotope-labeled in situ hybridization histochemistry ISHH. We detected mRNAs for BLT1 and CysLT2 in the DRG, but not for BLT2 and CysLT1. CysLT2 mRNA was preferentially expressed by small sized DRG neurons about 36% of total neurons, whereas BLT1 mRNA was expressed by non-neuronal cells. Double labeling analysis of CysLT2 with NF-200, calcitonin gene-related peptide CGRP, isolectin B4 IB4, transient receptor potential vanilloid subfamily 1 TRPV1 and P2X3 receptor revealed that many CysLT2-labeled neurons were localized with unmyelinated and non-peptidergic neurons, and interestingly, CysLT2 mRNA heavily co-localized with TRPV1 and P2X3-positive neurons. Intraplantar injection of LTC4, a CysLT2 receptor agonist, itself did not induce the thermal hyperalgesia, spontaneous pain behaviors or swelling of hind paw. However, pretreatment of LTC4 remarkably enhanced the painful behaviors produced by alpha, beta-methylene adenosine 5-triphosphate αβ-me-ATP, a P2X3 receptor agonist.

ConclusionsThese data suggests that CysLT2 expressed in DRG neurons may play a role as a modulator of P2X3, and contribute to a potentiation of the neuronal activity following peripheral inflammation.

Electronic supplementary materialThe online version of this article doi:10.1186-1744-8069-6-57 contains supplementary material, which is available to authorized users.

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Autor: Masamichi Okubo - Hiroki Yamanaka - Kimiko Kobayashi - Tetsuo Fukuoka - Yi Dai - Koichi Noguchi

Fuente: https://link.springer.com/







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