"Pain hypersensitivity: Identification of molecular targets" Fernando Cervero 博士（加拿大McGill大学艾伦•爱德华兹疼痛研究中心）-2012.5.15

时间:2012年5月15日 10:00

地点：理科大楼A510

报告题目：Pain hypersensitivity: Identification of molecular targets

报告人：Fernando Cervero 博士 加拿大McGill大学艾伦•爱德华兹疼痛研究中心

报告人简介：加拿大McGill大学艾伦•爱德华兹疼痛研究中心主任；麻醉学教授；生理学、神经学客座教授。研究方向为疼痛和镇痛的神经生物学机制，目前的研究主要集中于由内脏疾病所导致的疼痛感受性增强的神经机制。其研究成果论文发表超过200多篇，并编辑多本探讨疼痛机制的书籍。由于其突出的研究工作，被选为欧洲科学院院士，是《欧洲疼痛杂志》创始人之一、主编，《疼痛》杂志副主编，《欧洲神经科学杂志》疼痛栏目编辑。

报告简介：Sensitization of visceral nociceptors is influenced by the microenvironment where the nociceptors are located and the function of non-neural epithelial cells of the organ in question. Recent data shows that modulation of visceral nociceptors with cannabinoid receptor agonists can reduce visceral pain and hyperalgesia. There is also considerable evidence in support of an enhanced excitability of spinal cord neurons as the mechanism responsible for the manifestation of visceral hyperalgesic states and several neurotransmitter systems have been implicated in the generation of this central hyperexcitability. We have shown that trafficking of the AMPA subclass of glutamate receptor, from the cytosol to the membrane can account for the development of central hyperexcitability states of visceral nociceptive pathways.The importance of the GABAergic system in spinal nociceptive processing has also been appreciated but we have only recently begun to understand how this system is modulated by the regulation of anion gradients. We have shown that a cation-chloride cotransporter, NKCC1 is involved in the generation of the touch-evoked pain component of visceral hyperalgesia. Finally, increases in central excitability can also account for the enhanced pain sensitivity shown in functional abdominal pain disorders. We have identified an estrogen-dependent abdominal hyperalgesic state that can be induced by ovariectomy of adult mice and in which several markers of spinal cord excitability are over expressed. Therefore hormonal dysfunction can also contribute to generate visceral hyperalgesic states.