摘要
目的:本实验观察胆囊收缩素(CCK)在福尔马林致痛大鼠感觉信息传递中的作用。方法:用免疫组织化学技术,分别观察阴性对照、生理盐水、福尔马林致痛后1 h和福尔马林致痛后3 h大鼠脊髓背角的感觉神经元神经肽CCK表达的变化。结果:大鼠足底注射福尔马林1 h后,脊髓背角Ⅰ、Ⅱ层神经元CCK表达阳性细胞数明显增加(P<0.01),且注射侧阳性细胞数明显高于非注射侧。注射福尔马林1 h后,注射侧和非注射侧CCK表达阳性细胞的半定量光密度均值分别是0.397±0.014和0.295±0.007,差异有显著性(P<0.01);注射福尔马林3 h后,注射侧和非注射侧脊髓背角CCK表达阳性细胞的半定量光密度均值分别是0.366±0.009和0.303±0.005,差异仍有显著性(P<0.01)。结论:福尔马林致痛大鼠脊髓CCK表达阳性细胞的半定量光密度均值增加,进一步证实CCK在炎性痛信息传递通路的多个环节中参与了痛觉调制。
Aim: CCK is one of the strongest endogenous anti-opioid substances and suppresses morphine tolerance which results from long term use of morphine. This study explores the modulatory effect of CCK on pain formalin-induced. Methods: The effect of formalin-induced pain on CCK immunoreactivity in rat sensory neurons was observed through immunohistochemistry technique. Results: After 1 h of subcutaneous injection of formalin in one paw of rats, the number of positive neurons of CCK immunoreactivity in spinal cord neurons was obviously increased and greater than that of non-injection side( P 〈 0.01 ). The semi-quantitative optical density average values of CCK immunoreactivity neurons were 0.397 ± 0.014 and 0.295 ±0.007 in injection side and non-injection side respectively, the difference was obvious( P 〈 0.01). After 3 h of subcutaneous injection of formalin in one paw of rats, the semi-quantitative optical density average values of CCK immunoreactivity neurons were 0.366 ± 0.009 and 0. 303 + 0.005 in injection side and noninjection side respectively, the difference was significant( P 〈 0.01). Conelusion: Formalin-induced pain can significantly change semi-quantitative optical density average value of CCK immunoractivity in spinal cord neurons, this indicates CCK participates in modulation of pain.
出处
《中国应用生理学杂志》
CAS
CSCD
北大核心
2009年第2期217-220,共4页
Chinese Journal of Applied Physiology
基金
石河子大学高层人才项目(RCZX200546)
石河子大学校级课题(200543)