發(fā)布時(shí)間：2018-02-27 15:48

  本文關(guān)鍵詞： 帕金森病 電刺激 腦橋核 蒼白球 微電泳 谷氨酸 γ氨基丁酸　出處：《遼寧醫(yī)學(xué)院》2014年碩士論文　論文類型：學(xué)位論文

【摘要】：目的 通過(guò)觀察低頻電刺激帕金森�。≒arkinsons’s disease，PD）模型大鼠腳橋核（pedunculopontine nucleus，PPN）及微電泳神經(jīng)遞質(zhì)對(duì)蒼白球內(nèi)側(cè)部（GPi）神經(jīng)元放電的影響，探討低頻電刺激PPN治療PD的作用機(jī)制。為臨床采用電刺激治療帕金森病提供實(shí)驗(yàn)依據(jù)。 方法 將30只SD大鼠隨機(jī)分為對(duì)照組（10只）和PD模型組（20只）。大鼠腦右側(cè)炓質(zhì)致密部注入6-羥基多巴胺建立PD模型；自行拉制7管玻璃微電極，采用細(xì)胞外單位記錄方法觀察記錄低頻電刺激PPN、微電泳谷氨酸（Glu）及其受體阻斷劑MK-801、γ-氨基丁酸（GABA）及其受體阻斷劑荷包牡丹堿（BIC）、乙酰膽堿（ACh）及其受體阻斷劑阿托品（ATR）對(duì)PD大鼠GPi神經(jīng)元自發(fā)放電的影響。 結(jié)果 PD組大鼠GPi神經(jīng)元基礎(chǔ)放電頻率較對(duì)照組增高（P＜0.05）；低頻電刺激PPN，對(duì)照組及PD組大鼠GPi神經(jīng)元反應(yīng)均以抑制為主，且平均放電頻率均較刺激前明顯降低（P＜0.01）；微電泳Glu、BIC和ACh對(duì)神經(jīng)元有興奮作用，，而微電泳MK-801、GABA和阿托品對(duì)神經(jīng)元有抑制作用。在微電泳BIC的興奮作用的基礎(chǔ)上低頻電刺激PPN使GPi神經(jīng)元放電頻率增高，而在微電泳MK-801和ATR抑制作用的基礎(chǔ)上低頻刺激PPN使GPi神經(jīng)元放電頻率進(jìn)一步降低。 結(jié)論 低頻電刺激PPN可抑制大鼠GPi神經(jīng)元的放電活動(dòng)，可能是通過(guò)調(diào)節(jié)投射到GPi神經(jīng)元的Glu、GABA和Ach能神經(jīng)通路實(shí)現(xiàn)的，而且GABA能作用更加明顯。
[Abstract]:Purpose. To observe the effects of low frequency electrical stimulation of parkinsonssus disease (PDD) on the discharge of GPiG neurons in the medial globus pallidus of the rat model of Podonus pedunculata (PPN) and microelectrophoretic neurotransmitters (microelectrophoretic neurotransmitters). To explore the mechanism of low frequency electrical stimulation (PPN) in the treatment of PD and to provide experimental evidence for clinical treatment of Parkinson's disease. Method. Thirty SD rats were randomly divided into control group (n = 10) and PD model group (n = 20). The low frequency electrical stimulation (PPN, microelectrophoresis glutamate Glu), its receptor blockers MK-801, 緯 -aminobutyric acid (GABA) and its receptor blockers bicarbonate, acetylcholine (ache) and its receptor blocker atropine (ATR) were observed by extracellular unit recording method. Effect on spontaneous discharges of GPi neurons in PD rats. Results. The basal discharge frequency of GPi neurons in PD group was higher than that in control group (P < 0.05), and the response of GPi neurons to low frequency electrical stimulation was mainly inhibited in control group and PD group. The average discharge frequency was significantly lower than that before stimulation (P < 0.01), and microelectrophoretic gel electrophoresis (GluBIC) and ACh could excite neurons. On the other hand, microelectrophoretic MK-801GABA-GABA and atropine inhibited neurons. On the basis of the excitatory effect of microelectrophoretic BIC, low frequency electrical stimulation of PPN increased the firing frequency of GPi neurons. On the basis of inhibition of MK-801 and ATR by microelectrophoretic, low frequency stimulation of PPN further decreased the firing frequency of GPi neurons. Conclusion. Low frequency electrical stimulation of PPN could inhibit the discharges of GPi neurons in rats, possibly by regulating the Glu-GABA and Ach energy pathways projected to GPi neurons, and the effect of GABA was more obvious.
【學(xué)位授予單位】：遼寧醫(yī)學(xué)院
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2014
【分類號(hào)】：R742.5

【共引文獻(xiàn)】

相關(guān)期刊論文 前2條

1 范志雄;陳劍春;吳曦;胡小吾;;腳橋核的功能和臨床應(yīng)用研究進(jìn)展[J];臨床神經(jīng)外科雜志;2014年04期

2 郭佳;林宇涵;李W

本文編號(hào)：1543308