"Pain hypersensitivity: Identification of molecular targets" Fernando Cervero 博士（加拿大McGill大學艾倫•愛德華茲疼痛研究中心）-2012.5.15

時間:2012年5月15日 10:00

地點：理科大樓A510

報告題目：Pain hypersensitivity: Identification of molecular targets

報告人：Fernando Cervero 博士 加拿大McGill大學艾倫•愛德華茲疼痛研究中心

報告人簡介：加拿大McGill大學艾倫•愛德華茲疼痛研究中心主任；麻醉學教授；生理學、神經學客座教授。研究方向為疼痛和鎮痛的神經生物學機制，目前的研究主要集中于由內臟疾病所導致的疼痛感受性增強的神經機制。其研究成果論文發表超過200多篇，并編輯多本探討疼痛機制的書籍。由于其突出的研究工作，被選為歐洲科學院院士，是《歐洲疼痛雜志》創始人之一、主編，《疼痛》雜志副主編，《歐洲神經科學雜志》疼痛欄目編輯。

報告簡介：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.