损毁炎症大鼠下丘脑弓状核对痛觉过敏的影响

发布时间：2018-07-09 22:12

本文选题：下丘脑弓状核 + 佐剂炎症　；参考：《苏州大学》2012年硕士论文

【摘要】：目的：本实验旨在观察损毁炎症大鼠下丘脑弓状核（hypothalamic arcuatenucleus, ARC）对炎症大鼠痛觉过敏的影响，并通过其对脊髓水平c-fos表达的影响来探讨ARC对痛觉过敏的下行调制。方法：用完全弗氏佐剂（complete Freund’s adjuvant, CFA）建立大鼠外周组织炎症模型；用辐射热-缩腿法测定炎症大鼠热痛阈的变化；用von Frey法测定机械痛阈的变化；用免疫组织化学方法检测大鼠脊髓L4和L5节段背角中的c-fos表达；用新生期注射谷氨酸单钠(monosodium glutamate, MSG)破坏ARC神经元胞体和电解损毁ARC两种方法损毁ARC。结果：（1）大鼠在注射CFA后即发生痛觉过敏(热痛阈和机械痛阈明显降低)，3h达到高峰，到3天有所恢复并且稳定维持痛觉过敏状态，一直维持到本实验观察的第十七天，到第二十一天才基本恢复。（2）注射过MSG大鼠在注射CFA后3h，热痛阈和机械痛阈均明显降低，，出现痛觉过敏，但其痛阈降低的幅度明显小于注射高渗盐水的假损毁CFA组。MSG大鼠和注射高渗盐水的假损毁组在注射生理盐水前后，热痛阈和机械痛阈都没有明显Y 化。提示MSG破坏ARC神经元胞体后，减轻了CFA引起的痛觉过敏。（3）MSG大鼠在注射CFA后3h，在L4-L5段脊髓背角I-II层和V-VI层所诱发的Fos免疫反应阳性细胞数明显少于高渗盐水的假损毁对照组，提示MSG破坏ARC神经元胞体后，脊髓背角神经元兴奋性降低，对外周炎症的反应减弱。(4) CFA炎症大鼠在电解损毁ARC之后，其热痛阈和机械痛阈与假损k雷橄啾龋飨陨仙崾镜缃馑鸹貯RC也能减轻CFA引起的痛觉过敏。结论：在外周存在CFA炎症条件下，两种方法损毁ARC都能减轻痛觉过敏。提示ARC参与外周组织炎症引起的痛觉过敏。由于损毁ARC都能减轻痛觉过敏和下调脊髓背角的Fos表达，提示在炎症条件下，ARC中的神经元对脊髓背角的兴奋性和痛觉过敏的发生有下行易化作用。
[Abstract]:Aim: to observe the effect of (hypothalamic arcuatenucleus, ARC on hyperalgesia in inflammatory rats, and to explore the down-regulation of hyperalgesia by c-fos expression in spinal cord. Methods: the inflammatory model of peripheral tissue was established by complete Freundsadjuvant (CFA), the changes of thermal pain threshold in inflammatory rats were measured by radiation heat contraction method, the changes of mechanical pain threshold were measured by von Frey method. Immunohistochemical method was used to detect the expression of c-fos in the dorsal horn of L4 and L5 segments of rat spinal cord. Results: (1) the hyperalgesia (thermal pain threshold and mechanical pain threshold) reached its peak at 3 h after CFA injection in rats, and recovered at 3 days and maintained a stable state of hyperalgesia until the 17th day of the experiment. By the 21 day, the thermal pain threshold and mechanical pain threshold were significantly decreased, and hyperalgesia was found in the rats. However, the decrease of pain threshold was significantly lower than that in CFA group. MSG group and sham damage group before and after injection of saline. The thermal pain threshold and mechanical pain threshold did not change significantly before and after injection of normal saline. The results suggest that MSG can reduce the hyperalgesia induced by CFA after destroying the cell bodies of ARC neurons. (3) the number of Fos immunoreactive positive cells induced by I-II layer and V-VI layer of spinal dorsal horn in MSG rats at 3 h after CFA injection was significantly lower than that in the sham damage control group with hypertonic saline. It was suggested that the excitability of spinal dorsal horn neurons decreased and the response of peripheral inflammation was weakened after MSG destroyed the cell bodies of ARC neurons. (4) after electrolytic lesion of ARC, the thermal and mechanical pain thresholds and pseudo-damage klystrin caries were found in CFA inflammatory rats. What is it? Hypersensitivity caused by CFA can also be alleviated by mirror-droplet storage RC. Conclusion: in the presence of CFA inflammation, both methods can reduce hyperalgesia. The results suggest that ARC is involved in hyperalgesia caused by peripheral tissue inflammation. As the lesion of ARC can reduce the hyperalgesia and down-regulate the expression of Fos in the dorsal horn of the spinal cord, it is suggested that the neurons in the ARC can facilitate the occurrence of excitability and hyperalgesia in the dorsal horn of the spinal cord under inflammatory conditions.
【学位授予单位】：苏州大学
【学位级别】：硕士
【学位授予年份】：2012
【分类号】：R363

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