本文選題：癲癇 + 三叉神經(jīng)電刺激��； 參考：《安徽醫(yī)科大學》2014年碩士論文

【摘要】：目的 觀察經(jīng)皮三叉神經(jīng)慢性電刺激(trigeminal nerve chronic stimulation，TCNS)對匹羅卡品誘導的慢性癲癇大鼠海馬和皮層內(nèi)囊泡型谷氨酸轉運體-（1vesicularglutamate transporter1, VGLUT1）與囊泡型γ-氨基丁酸轉運體（vesicular GABAtransporter，VGAT）表達的影響，探討三叉神經(jīng)電刺激治療癲癇的可能機制。 方法 選用成年健康雄性SD大鼠150只，隨機選出100只建立匹羅卡品慢性癲癇模型，然后將達到癲癇持續(xù)狀態(tài)（Status epilepticus，SE）的實驗大鼠隨機分為模型(Pilo)組和經(jīng)皮三叉神經(jīng)電刺激(TNS)組；正常對照（Control）組給予同劑量的生理鹽水代替匹羅卡品腹腔注射，隨后Control組和Pilo組均給予為期一個月的經(jīng)皮三叉神經(jīng)假性電刺激、TNS組給予為期一個月的真性電刺激。各組大鼠均于經(jīng)皮三叉神經(jīng)電刺激結束后24h、72h、7d、14d、28d取材，通過免疫熒光雙標和Western blot方法，，分析海馬和皮層內(nèi)VGLUT1和VGAT的表達情況。所得數(shù)據(jù)以均數(shù)±標準差(x±s)表示，組間均數(shù)比較采用單因素方差(One-way ANOVA)分析,以P0.05為差異有統(tǒng)計學意義，P0.01為差異有顯著統(tǒng)計學意義。 結果 1.VGLUT1在海馬和皮層內(nèi)的表達 TNS組和Pilo組大鼠海馬、皮層內(nèi)VGLUT1的表達較Control組均明顯增加，總體上均呈先升高后下降的趨勢，約在72h左右達到高峰。在24h時，TNS組大鼠海馬和皮層內(nèi)VGLUT1的表達均明顯高于Pilo組（P0.01）,而在以后各個時間點均低于Pilo組（P0.01，P0.05）；TNS組大鼠海馬內(nèi)VGLUT1的表達量在28d時、皮層內(nèi)在14d和28d時與Control組相比差異無統(tǒng)計學意義（P0.05）,但與Pilo組相比差異均有統(tǒng)計學意義（P0.05）。 2.VGAT在海馬和皮層內(nèi)的表達 TNS組和Pilo組大鼠海馬、皮層內(nèi)VGAT的表達較Control組均明顯增加，在72h之前VGAT的表達量逐漸增加，約在72h左右達到高峰，隨后開始下降。在72h時，TNS組大鼠海馬和皮層內(nèi)VGAT的表達量均明顯低于Pilo組（P0.01）,而在24h、7d、14d、28d時均明顯高于Pilo組（P0.01，P0.05）。在28d時，Pilo組大鼠海馬和皮層內(nèi)VGAT的表達量與Control組相比差異無統(tǒng)計學意義（P0.05）、但與TNS組相比差異仍有統(tǒng)計學意義（P0.05）。 結論 在匹羅卡品誘導的慢性癲癇大鼠模型形成過程中，予以經(jīng)皮三叉神經(jīng)慢性電刺激處理減弱了腦的興奮性機制、增強了其內(nèi)源性抑制性機制，從而使腦的興奮易感性降低；這一作用機制可能與腦內(nèi)囊泡型谷氨酸轉運體-1先增多后減少、囊泡型γ-氨基丁酸轉運體明顯增多有關，這可能是三叉神經(jīng)電刺激減少癲癇發(fā)作的機制之一。
[Abstract]:Purpose The effects of trigeminal nerve chronic stimulation on the expression of vesicular-glutamate transporter-1 (VGLUT1) and vesicular GABA transporter-1 (VGLUT1) in hippocampus and cortex of pilocarpine induced chronic epilepsy rats were observed. To explore the possible mechanism of trigeminal nerve stimulation in the treatment of epilepsy. Method A total of 150 adult male Sprague-Dawley (SD) rats were randomly selected to establish pilocarpine chronic epilepsy model, and then the experimental rats with status epilepticus were randomly divided into two groups: model Pilo group and percutaneous trigeminal nerve stimulation group (TNSgroup). The normal control group was given the same dose of normal saline instead of pilocarpine intraperitoneal injection, then the Control group and the Pilo group were given one month of percutaneous trigeminal nerve pseudoelectric stimulation for one month. The expression of VGLUT1 and VGAT in hippocampus and cortex were analyzed by immunofluorescence double labeling and Western blot method at 24 h, 72 h, 7 d, 14 d and 28 d after the end of percutaneous trigeminal nerve stimulation. The data were expressed as mean 鹵standard deviation (x 鹵s). One-way ANOVAanalysis was used to compare the mean between groups. There was a significant difference between the two groups (P0.05) (P 0.01). Result Expression of 1.VGLUT1 in hippocampus and cortex The expression of VGLUT1 in hippocampus and cortex of TNS group and Pilo group was significantly higher than that of Control group, and the expression of VGLUT1 increased first and then decreased, reaching the peak at about 72 h. At 24 hours, the expression of VGLUT1 in hippocampus and cortex was significantly higher in the group of Pilo than that in the group of Pilo, and the expression of VGLUT1 in the hippocampus was lower than that in the group of Pilo at every time point, and the expression of VGLUT1 in the hippocampus of the rats in the group of Pilo was lower than that in the group of P0.01and P0.05 at 28d. There was no significant difference between the cortex and the Control group on the 14th and 28th days, but there was significant difference between the cortex and the Pilo group (P 0.05). Expression of 2.VGAT in hippocampus and cortex The expression of VGAT in hippocampus and cortex of TNS group and Pilo group was significantly higher than that of Control group. The expression of VGAT increased gradually before 72 h, reached the peak at about 72 h, then began to decrease. At 72 h, the expression of VGAT in hippocampus and cortex of rats in TNS group was significantly lower than that in Pilo group (P 0.01), and was significantly higher than that in Pilo group at 14 d (14 d) at 24 h. On the 28th day, the expression of VGAT in hippocampus and cortex of rats in the Pilo group was not significantly different from that in the Control group (P 0.05), but there was still a significant difference compared with the TNS group. Conclusion In the course of the formation of pilocarpine induced chronic epilepsy rat model, the chronic electrical stimulation of the trigeminal nerve weakened the excitability mechanism of brain, enhanced its endogenous inhibitory mechanism, and reduced the susceptibility to brain excitability. This mechanism may be related to the increase of vesicular glutamate transporter -1 and the decrease of vesicular type 緯 -aminobutyric acid transporter, which may be one of the mechanisms of trigeminal electrical stimulation to reduce epileptic seizures.
【學位授予單位】：安徽醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2014
【分類號】：R742.1

【參考文獻】

相關期刊論文 前3條

1 李敏;孔德虎;許奇;王烈成;;顳葉癲癇大鼠不同時期海馬和皮層氨基酸類遞質的變化[J];安徽醫(yī)科大學學報;2010年02期

2 張慧敏;李良勇;李家林;王玉;;經(jīng)皮三叉神經(jīng)電刺激預處理對戊四氮致癇大鼠海馬谷氨酸脫羧酶表達的影響[J];安徽醫(yī)科大學學報;2011年08期

3 黃琳;王玉;;偏頭痛與癲癇關系的最新進展[J];中華臨床醫(yī)師雜志(電子版);2011年16期

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