前庭損傷急性期低血壓興奮MVN的NMDA受體機制
發(fā)布時間:2018-05-24 12:23
本文選題:急性低血壓 + 前庭神經(jīng)內(nèi)側(cè)核 ; 參考:《延邊大學》2011年碩士論文
【摘要】:有研究報道,在麻醉動物靜脈注射硝普鈉(Sodium nitroprusside, SNP)誘發(fā)急性低血壓時,流經(jīng)末梢前庭器官的血流量與血壓的降低呈正相關,使前庭神經(jīng)傳入沖動增加,釋放興奮性神經(jīng)遞質(zhì)—谷氨酸(Glutamate, Glu),來興奮前庭神經(jīng)內(nèi)側(cè)核(medial vestibular nucleus, MVN),并可使MVN區(qū)c-Fos蛋白表達增加。本研究利用免疫組織化學方法和藥理學方法,在一側(cè)外周前庭器官損傷急性期清醒大鼠,觀察了急性低血壓時前庭神經(jīng)內(nèi)側(cè)核區(qū)c-Fos蛋白的表達情況,并探討了其可能的Glu-NMDA受體機制。 選擇雄性Wistar系清潔級大鼠96只,體重在250±30g,隨機分為三個大組,即前庭器官正常組、單側(cè)前庭器官破壞組、NMDA受體組。前庭器官正常組又分對照組(n=6)和實驗組(n=6),分別靜脈注射生理鹽水和硝普鈉誘發(fā)急性低血壓;前庭器官破壞組首先用對氨基苯砷酸鹽單純破壞外周前庭器官6、12、24、48、72h后觀察MVN區(qū)c-Fos蛋白表達的情況,進而再分為對照組和實驗組,觀察外周前庭器官假破壞與真破壞后急性低血壓對MVN區(qū)c-Fos蛋白表達的影響;NMDA受體組分為NMDA受體激動劑組和阻斷劑組,分別向側(cè)腦室注射NMDA和MK-80110min后,觀察了急性低血壓的效應,對照組為人工腦脊液代替激動激或阻斷劑、生理鹽水代替硝普鈉。各組實驗均在動物清醒狀態(tài)下進行。 結(jié)果如下: 1.在正常動物誘發(fā)急性低血壓后MVN區(qū)c-Fos蛋白有明顯表達,但在對照組則無明顯表達。 2.單純破壞一側(cè)外周前庭器官6、24、48、72h時,破壞同側(cè)MVN區(qū)c-Fos蛋白無明顯表達,但在其對側(cè)則有明顯的表達,尤其是48h最為顯著。而在破壞12h時呈現(xiàn)為反向表達,即損傷同側(cè)表達增多,而損傷對側(cè)僅低水平表達。 3.破壞單側(cè)前庭器官48h后誘發(fā)急性低血壓時,破壞同側(cè)MVN區(qū)c-Fos蛋白無明顯表達,但對側(cè)有明顯表達。破壞單側(cè)前庭器官后靜脈注射生理鹽水的對照組則較實驗組相比表達不甚明顯,兩者之間有顯著性差異。在其對照組,即進行假前庭破壞后誘發(fā)急性低血壓后,則表現(xiàn)為兩側(cè)MVN區(qū)c-Fos蛋白對稱性分布,與實驗組相比有顯著性差異。 4.正常動物側(cè)腦室注射Glu受體興奮劑(NMDA),雙側(cè)MVN區(qū)均有明顯的c-Fos蛋白表達,與側(cè)腦室注射人工腦脊液的對照組相比有顯著性差異。 5.側(cè)腦室注射阻斷劑(MK-801)后注射SNP誘發(fā)急性低血壓,雙側(cè)MVN區(qū)只見少量的c-Fos表達,而在側(cè)腦室注射人工腦脊液后誘發(fā)急性低血壓,雙側(cè)MVN區(qū)則可見對稱性的c-Fos蛋白表達增加,與生理鹽水對照組相比未見明顯差異。 結(jié)論: 1.清醒動物破壞一側(cè)前庭器官早期,除12h時損傷側(cè)MVN區(qū)c-Fos蛋白表達多于對側(cè)以外,6、24、48、72h損傷對側(cè)多于損傷側(cè),而且48h表達最明顯; 2.清醒動物急性低血壓誘發(fā)的MVN興奮可能有Glu的NMDA受體參與。
[Abstract]:It has been reported that when sodium nitroprusside (SNPs) is injected intravenously into anesthetized animals to induce acute hypotension, the blood flow through vestibular organs is positively correlated with the decrease of blood pressure, which increases the afferent impulse of vestibular nerve. The release of excitatory neurotransmitter glutamate Glutamate (Glutamate) was used to excite medial vestibular nucleus, MVNs in medial vestibular nucleus, and to increase the expression of c-Fos protein in MVN region. In this study, immunohistochemical and pharmacological methods were used to observe the expression of c-Fos protein in medial vestibular nucleus during acute stage of peripheral vestibular organ injury in rats with acute hypotension. The possible mechanism of Glu-NMDA receptor was discussed. 96 male Wistar clean grade rats, weighing 250 鹵30 g, were randomly divided into three groups: normal vestibular organ group and unilateral vestibular organ destruction group. The normal vestibular organ group was divided into control group (n = 6) and experimental group (n = 6). The acute hypotension was induced by intravenous injection of normal saline and sodium nitroprusside respectively. In the vestibular organ destruction group, the expression of c-Fos protein in the MVN region was observed 72 hours after the destruction of the peripheral vestibular organ with p-aminobenzene arsenate alone, and was further divided into two groups: control group and experimental group. To observe the effect of acute hypotension on the expression of c-Fos protein in MVN region after peripheral vestibular organ pseudodestruction and true destruction, NMDA receptor groups were divided into NMDA receptor agonist group and blocker group. The effect of acute hypotension was observed after injecting NMDA and MK-80110min into lateral ventricle, respectively. The control group was treated with artificial cerebrospinal fluid (CSF) instead of stimulation or blocking agent and saline as sodium nitroprusside. All the experiments were carried out in the conscious state of the animals. The results are as follows: 1. The expression of c-Fos protein in the MVN region was significant after acute hypotension induced by normal animals, but not in the control group. 2. No significant expression of c-Fos protein was found in ipsilateral MVN region after the destruction of the unilateral vestibular organ 62448h for 72 h, but there was obvious expression in the contralateral side, especially at 48h. The reverse expression was found at 12 h after injury, that is, the ipsilateral expression was increased, but the contralateral expression was only low. 3. When acute hypotension was induced 48 hours after unilateral vestibular organ destruction, there was no obvious expression of c-Fos protein in ipsilateral MVN region, but obvious expression in contralateral side. The expression of normal saline after destroying unilateral vestibular organs in the control group was not obvious compared with the experimental group, and there was a significant difference between the two groups. After acute hypotension was induced by pseudovestibular destruction in the control group, the distribution of c-Fos protein in the bilateral MVN region was symmetrically distributed, which was significantly different from that in the experimental group. 4. In normal animals, the expression of c-Fos protein in the bilateral MVN region was significantly higher than that in the control group injected with artificial cerebrospinal fluid (ACSF) by intraventricular injection of Glu receptor stimulant (NMDAA). 5. Acute hypotension induced by SNP was induced by intraventricular injection of blocker MK-801. Only a small amount of c-Fos was expressed in bilateral MVN region, while acute hypotension was induced by intracerebroventricular injection of artificial cerebrospinal fluid (ACSF). Symmetrical expression of c-Fos protein was observed in bilateral MVN region. There was no significant difference compared with normal saline control group. Conclusion: 1. At the early stage of destroying one vestibular organ, the expression of c-Fos protein in the MVN region of the injured side was higher than that in the contralateral side at 72 h after injury, and the expression was the most obvious at 48 h. 2. MVN stimulation induced by acute hypotension in conscious animals may involve Glu NMDA receptor.
【學位授予單位】:延邊大學
【學位級別】:碩士
【學位授予年份】:2011
【分類號】:R363
【引證文獻】
相關碩士學位論文 前1條
1 李麗威;急性低血壓誘發(fā)MVN區(qū)pERK1/2表達的NMDA受體機制研究[D];延邊大學;2012年
,本文編號:1929035
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