Cinnamaldehyde induces a TRPA1-mediated nociceptive behavior in planarians.

IF 2.5 4区 医学 Q3 NEUROSCIENCES Neuroscience Letters Pub Date : 2024-11-14 DOI:10.1016/j.neulet.2024.138041
Rémy Morana, Bénédicte Darbon, Lalee Herrmann, Yannick Menger, Guillaume Reho, Hervé Cadiou
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Abstract

Nociception is defined as "the neural process of encoding noxious stimuli" by the International Association for the Study of Pain (IASP). Nociception relies on detecting noxious stimuli arising from a potentially or actually tissue-damaging event via specialized cells called nociceptors. In planarians, nociceptive behavior is often indicated by a 'scrunching' gait, in contrast to the usual gliding behavior displayed in normal conditions. The present study extends our previous study Reho et al. (2024) by testing a new potentially irritant molecule, Cinnamaldehyde (CA), which could induce scrunching gaits. We reproduced the nociceptive chemical tests from our previous study using CA instead of Allyl isothiocyanate (AITC) on Girardia dorotocephala (Gd) implementing an open field behavioral analysis. CA induced a dose-dependent increase in scrunching gait similar to the action of AITC and was expectedly partially suppressed by morphine and meloxicam. Knocking down the expression of the Gd-TRPA1 ion channel by RNA interference also suppressed the behavioral reaction to the molecule. In conclusion, we demonstrated that CA induced a nociceptive behavior in planarians through an action on the ion channel TRPA1. SIGNIFICANCE STATEMENT: In this article, we provide evidence that cinnamaldehyde induces a nociceptive behavior through a direct action in an invertebrate model (flatworm) much in the same way that in vertebrates.

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肉桂醛诱导扁形动物产生 TRPA1 介导的痛觉行为
国际疼痛研究协会(IASP)将痛觉定义为 "编码有害刺激的神经过程"。痛觉依赖于通过称为 "痛觉感受器 "的特化细胞来检测由潜在或实际的组织损伤事件引起的有害刺激。在扁形动物中,痛觉行为通常表现为 "抓挠 "步态,这与正常情况下的滑行行为截然不同。本研究扩展了 Reho 等人(2024 年)之前的研究,测试了一种新的潜在刺激性分子肉桂醛(Cinnamaldehyde,CA),它可以诱导抓挠步态。我们用 CA 代替异硫氰酸烯丙酯(AITC),在 Girardia dorotocephala(Gd)上重现了之前研究中的痛觉化学测试,并进行了开阔地行为分析。与 AITC 的作用类似,CA 会诱发剂量依赖性的抓挠步态增加,吗啡和美洛昔康也会部分抑制这种增加。通过 RNA 干扰阻断 Gd-TRPA1 离子通道的表达也抑制了对该分子的行为反应。总之,我们证明了 CA 是通过对 TRPA1 离子通道的作用来诱导扁形动物的痛觉行为的。意义声明:在这篇文章中,我们提供了肉桂醛在无脊椎动物模型(扁形虫)中通过直接作用诱导痛觉行为的证据,其方式与在脊椎动物中诱导痛觉行为的方式非常相似。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Neuroscience Letters
Neuroscience Letters 医学-神经科学
CiteScore
5.20
自引率
0.00%
发文量
408
审稿时长
50 days
期刊介绍: Neuroscience Letters is devoted to the rapid publication of short, high-quality papers of interest to the broad community of neuroscientists. Only papers which will make a significant addition to the literature in the field will be published. Papers in all areas of neuroscience - molecular, cellular, developmental, systems, behavioral and cognitive, as well as computational - will be considered for publication. Submission of laboratory investigations that shed light on disease mechanisms is encouraged. Special Issues, edited by Guest Editors to cover new and rapidly-moving areas, will include invited mini-reviews. Occasional mini-reviews in especially timely areas will be considered for publication, without invitation, outside of Special Issues; these un-solicited mini-reviews can be submitted without invitation but must be of very high quality. Clinical studies will also be published if they provide new information about organization or actions of the nervous system, or provide new insights into the neurobiology of disease. NSL does not publish case reports.
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