M2 receptors exert analgesic action on DRG sensory neurons by negatively modulating VR1 activity

DeAngelisF.; MarinelliS.; FiorettiB.CatacuzzenoL.FrancioliniF.PavoneF.TataA.M.

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M2 receptors exert analgesic action on DRG sensory neurons by negatively modulating VR1 activity

机译：M2受体对DRG感官产生镇痛作用神经元由负调节VR1活动

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The peripheral application of the M2 cholinergic agonist arecaidine on sensory nerve endings shows anti-nociceptive properties. In this work, we analyze in vitro, the mechanisms downstream M2 receptor activation causing the analgesic effects, and in vivo the effects produced by M2 agonist arecaidine administration on nociceptive responses in a murine model of nerve growth factor (NGF)-induced pain. Cultured DRG neurons treated with arecaidine showed a decreased level of VR1 and SP transcripts. Conversely, we found an increased expression of VR1 and SP transcripts in DRG from M2/M4-/- mice compared to WT and M1-/- mice, confirming the inhibitory effect in particular of M2 receptors on SP and VR1 expression. Patch-clamp experiments in the whole-cell configuration showed that arecaidine treatment caused a reduction of the fraction of capsaicin-responsive cells, without altering the mean capsaicin-activated current in responsive cells. We also demonstrated that arecaidine prevents PKCε{lunate} translocation to the plasma membrane after inflammatory agent stimulation, mainly in medium-small sensory neurons. Finally, in mice, we have observed that intraperitoneal injection of arecaidine reduces VR1 expression blocking hyperalgesia and allodynia caused by NGF intraplantar administration. In conclusion, our data demonstrate that in vivo M2 receptor activation induces desensitization to mechanical and heat stimuli by a down-regulation of VR1 expression and by the inhibition of PKCε{lunate} activity hindering its translocation to the plasma membrane, as suggested by in vitro experiments. J. Cell. Physiol. 229: 783-790, 2014.

机译：M2的外围应用胆碱能受体激动剂arecaidine感觉神经末梢显示anti-nociceptive属性。分析体外,下游M2的机制受体激活导致镇痛影响,体内产生的影响平方米受体激动剂arecaidine疼痛的管理神经生长因子在鼠模型的反应因子(神经生长因子)全身疼痛。对待arecaidine显示水平下降VR1和SP的记录。表达的增加VR1和SP记录在DRG M2 / M4 - / -小鼠相比WTM1 - / -小鼠,确认的抑制作用特定的M2 SP和VR1受体表达式。全细胞表明arecaidine配置治疗分数的减少造成的capsaicin-responsive细胞,没有改变意味着capsaicin-activated电流响应细胞。防止PKCε{半月形的}易位的等离子体膜炎症剂刺激后,主要是在小批量感觉神经元。在小鼠中,我们观察到腹腔内注入arecaidine减少VR1表达式阻断痛觉过敏和神经生长因子引起的异常性疼痛intraplantar管理。数据表明,体内M2受体机械活化诱发脱敏和热刺激的下调VR1表达和抑制PKCε{半月形的}活动阻碍其易位等离子体膜,建议通过体外实验。2014.

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《Journal of Cellular Physiology》 |2014年第6期|783-790|共8页
作者
DeAngelisF.; MarinelliS.; FiorettiB.CatacuzzenoL.FrancioliniF.PavoneF.TataA.M.;
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Department of Biology and Biotechnologies C. Darwin, Sapienza University of Rome, Rome, Italy;

Department of Cell and Environmental Biology, University of Perugia, Perugia, Italy;

CNR, Cell Biology and Neurobiology Institute, Rome, Italy, IRCCS Fondazione Santa Lucia, Rome, Italy;

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arecaidine; Sensory Receptor Cells; muscarinic M2 receptorPlasma membraneHeat stimuliSensory Nerve Endings;

机译：arecaidine;感官受体细胞毒蕈碱的平方米receptorPlasma membraneHeat stimuliSensory神经结局;

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M2 receptors exert analgesic action on DRG sensory neurons by negatively modulating VR1 activity

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