Xenon fails to inhibit capsaicin-evoked CGRP release by nociceptors in culture

被引:5
|
作者
Calcott, Guy
White, John P. M.
Nagy, Istvan
机构
[1] Section of Anaesthetics and Pain Medicine and Intensive Care, Department of Surgery and Cancer and Faculty of Medicine, Imperial College London and Chelsea and Westminster Hospital, London SW10 9NH, 369, Fulham Road
关键词
Analgesia; CGRP; Nociceptors; Pain; Xenon; NITROUS-OXIDE; INFLAMMATORY PAIN; RECEPTOR; NEURONS; TRPV1; ANESTHESIA; CHANNELS; SITE; AMPA;
D O I
10.1016/j.neulet.2011.05.051
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
To investigate whether the xenon-induced inhibition of the transient receptor potential vanilloid type 1 (TRPV1) ion channel in rat dorsal root ganglion (DRG) neurons reduces nociceptive processing, we examined the effect of xenon in reducing the release of calcitonin gene-related peptide (CGRP) from those neurons. We found that exposure to xenon failed to effect a reduction of capsaicin-evoked CGRP release from cultured primary sensory neurons when stimulated by capsaicin. This finding suggests that xenon acts on several molecular targets on nociceptive primary sensory neurons, and that xenon's action on one, or more, of those targets serves to offset the inhibitory, pro-analgesic, effect of xenon on TRPV1. It is concluded that xenon may not produce any analgesic effect through peripheral nociceptors. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
引用
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页码:124 / 126
页数:3
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