本文選題：下丘腦弓狀核 + 佐劑炎癥�。� 參考：《蘇州大學(xué)》2012年碩士論文

【摘要】：目的：本實(shí)驗(yàn)旨在觀察損毀炎癥大鼠下丘腦弓狀核（hypothalamic arcuatenucleus, ARC）對炎癥大鼠痛覺過敏的影響，并通過其對脊髓水平c-fos表達(dá)的影響來探討ARC對痛覺過敏的下行調(diào)制。 方法：用完全弗氏佐劑（complete Freund’s adjuvant, CFA）建立大鼠外周組織炎癥模型；用輻射熱-縮腿法測定炎癥大鼠熱痛閾的變化；用von Frey法測定機(jī)械痛閾的變化；用免疫組織化學(xué)方法檢測大鼠脊髓L4和L5節(jié)段背角中的c-fos表達(dá)；用新生期注射谷氨酸單鈉(monosodium glutamate, MSG)破壞ARC神經(jīng)元胞體和電解損毀ARC兩種方法損毀ARC。 結(jié)果：（1）大鼠在注射CFA后即發(fā)生痛覺過敏(熱痛閾和機(jī)械痛閾明顯降低)，3h達(dá)到高峰，到3天有所恢復(fù)并且穩(wěn)定維持痛覺過敏狀態(tài)，一直維持到本實(shí)驗(yàn)觀察的第十七天，到第二十一天才基本恢復(fù)。（2）注射過MSG大鼠在注射CFA后3h，熱痛閾和機(jī)械痛閾均明顯降低，，出現(xiàn)痛覺過敏，但其痛閾降低的幅度明顯小于注射高滲鹽水的假損毀CFA組。MSG大鼠和注射高滲鹽水的假損毀組在注射生理鹽水前后，熱痛閾和機(jī)械痛閾都沒有明顯Y 化。提示MSG破壞ARC神經(jīng)元胞體后，減輕了CFA引起的痛覺過敏。（3）MSG大鼠在注射CFA后3h，在L4-L5段脊髓背角I-II層和V-VI層所誘發(fā)的Fos免疫反應(yīng)陽性細(xì)胞數(shù)明顯少于高滲鹽水的假損毀對照組，提示MSG破壞ARC神經(jīng)元胞體后，脊髓背角神經(jīng)元興奮性降低，對外周炎癥的反應(yīng)減弱。(4) CFA炎癥大鼠在電解損毀ARC之后，其熱痛閾和機(jī)械痛閾與假損k雷橄啾齲饗隕仙崾鏡緗饉鴰貯RC也能減輕CFA引起的痛覺過敏。 結(jié)論：在外周存在CFA炎癥條件下，兩種方法損毀ARC都能減輕痛覺過敏。提示ARC參與外周組織炎癥引起的痛覺過敏。由于損毀ARC都能減輕痛覺過敏和下調(diào)脊髓背角的Fos表達(dá)，提示在炎癥條件下，ARC中的神經(jīng)元對脊髓背角的興奮性和痛覺過敏的發(fā)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.
【學(xué)位授予單位】：蘇州大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2012
【分類號】：R363

【參考文獻(xiàn)】

相關(guān)期刊論文 前10條

1 卓敏;疼痛的神經(jīng)生物學(xué)——理解大腦機(jī)制及神經(jīng)疾病治療的機(jī)理[J];世界科技研究與發(fā)展;2005年01期

2 徐智策,蔣星紅;快反應(yīng)基因在神經(jīng)科學(xué)研究中的進(jìn)展與動態(tài)[J];生理科學(xué)進(jìn)展;1997年01期

3 郭試瑜,殷偉平,張惠琴,印其章;大鼠下丘腦弓狀核區(qū)在唇針鎮(zhèn)痛中的作用[J];生理學(xué)報(bào);1982年01期

4 端木肇夏 ,張躍進(jìn) ,張惠琴 ,印其章;刺激中縫背核和藍(lán)斑對下丘腦弓狀核區(qū)誘發(fā)電位的影響[J];生理學(xué)報(bào);1985年06期

5 陳起亮，李金華，周志菁，印其章;損毀或刺激垂體和下丘腦弓狀核對大鼠痛覺調(diào)制的影響[J];生理學(xué)報(bào);1995年05期

6 彭建明;朱奇;虞獻(xiàn)民;蔣星紅;;谷氨酸對大鼠離體下丘腦內(nèi)側(cè)基底部弓狀核神經(jīng)元電活動的影響[J];蘇州大學(xué)學(xué)報(bào)(醫(yī)學(xué)版);2008年03期

7 潘燕燕;龔珊;虞獻(xiàn)民;蔣星紅;;下丘腦弓狀核微量注射NMDA受體拮抗劑和蛋白激酶抑制劑對神經(jīng)病理性痛覺過敏的抑制作用[J];蘇州大學(xué)學(xué)報(bào)(醫(yī)學(xué)版);2010年02期

8 李瑋;龔珊;虞獻(xiàn)民;蔣星紅;;外周炎癥性疼痛誘導(dǎo)下丘腦弓狀核c-fos表達(dá)及其機(jī)制[J];蘇州大學(xué)學(xué)報(bào)(醫(yī)學(xué)版);2011年02期

9 李昕,宮澤輝,劉克良;酪氨酸蛋白激酶與突觸可塑性及學(xué)習(xí)記憶的關(guān)系[J];中國藥理學(xué)通報(bào);2005年02期

10 龔珊，矯勇益，殷偉平，印其章;新生期注射谷氨酸單鈉對刺激下丘腦弓狀核鎮(zhèn)痛作用的影響[J];神經(jīng)科學(xué);1994年01期

相關(guān)碩士學(xué)位論文 前1條

1 梁倩;Cobratoxin鎮(zhèn)痛及其機(jī)制的研究[D];蘇州大學(xué);2011年

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