Upregulation of transient receptor potential vanilloid 1 contributes to hyperalgesia in rats with pa

• 作 者: Guang-YinXU[1]JohnHWINSTON[2]MohanSHENOY[2]Huai-ZhiYIN[2]PankajJayPASRICHA[2]
• 机 构: The Jiangsu Key Laboratory of Neuroregeneration, Nantong University, Nantong 226001, China
• 出 处: 中国神经科学学会第四次会员代表大会暨第七届全国学术会议(The 7th Biennial Meeting and the
• 发表日期: 2007年期

　　The neurobiological basis of pancreatic hyperalgesia in chronic pancreatitis (CP) is poorly understood and treatment of pain in this condition remains empirical and often ineffective.We have previously developed a rat model of trinitrobenzene sulphonic acid (TNBS)-induced chronic pancreatitis that results in nociceptive sensitization in rats manifested by pancreatic hyperalgesia and referred somatic allodynia.The aim of this study was to investigate the molecular substrate of these changes,specifically focusing on the role of the transient receptor potential vanilloid subfamily 1 (TRPV 1).CP was induced in adult rats by a single intraductal injection of TNBS.Dorsal root ganglion (DRG) neurons innervating the pancreas were identified by Dil or cholera B toxin fluorescence labeling.TRPV 1 currents in pancreas-specific DRG neurons were measured using perforated patch-clamp techniques.RT-PCR was used to measure mRNA expression of TRPV 1 in pancreas-specific DRG neurons after laser capture microdissection (LCM).