天津医药
天津醫藥
천진의약
TIANJIN MEDICAL JOURNAL
2014年
8期
774-777
,共4页
郭佳%林宇涵%李垚%焦金菊
郭佳%林宇涵%李垚%焦金菊
곽가%림우함%리요%초금국
帕金森病%电刺激%脑桥脚被盖核%苍白球%谷氨酸%γ氨基丁酸%脑桥核%微电泳
帕金森病%電刺激%腦橋腳被蓋覈%蒼白毬%穀氨痠%γ氨基丁痠%腦橋覈%微電泳
파금삼병%전자격%뇌교각피개핵%창백구%곡안산%γ안기정산%뇌교핵%미전영
Parkinson disease%electric stimulation%pedunculopontine tegmental nucleus%globus pallidus%glutamic acid%gamma-aminobutyric acid%pedunculopontine pucleus%microiontophoresis
目的:通过观察低频电刺激帕金森病(PD)模型大鼠脚桥核(PPN)对苍白球内侧部(GPi)神经元放电的影响,探讨低频电刺激PPN治疗PD的作用机制。方法30只SD大鼠随机分为对照组和PD组各15只。大鼠脑右侧黑质致密部注入6-羟基多巴胺建立PD模型;采用细胞外记录方法,利用7管玻璃微电极记录观察低频电刺激、微电泳谷氨酸(Glu)及其受体阻断剂MK-801、γ-氨基丁酸(GABA)及其受体阻断剂荷包牡丹碱(BIC)对大鼠GPi神经元放电频率的影响。结果低频电刺激PPN,对照组及PD组大鼠GPi神经元反应均以抑制为主,且平均放电频率均较刺激前降低(P<0.01);微电泳Glu和BIC对神经元有兴奋作用,而微电泳MK-801和GABA对神经元有抑制作用。在微电泳BIC的兴奋作用的基础上低频电刺激PPN使神经元放电频率明显降低,而在微电泳MK-801抑制作用的基础上低频刺激PPN使神经元放电频率进一步降低。结论低频电刺激PPN可抑制GPi神经元活动,可能是通过调节投射到GPi神经元的Glu和GABA神经通路实现的。
目的:通過觀察低頻電刺激帕金森病(PD)模型大鼠腳橋覈(PPN)對蒼白毬內側部(GPi)神經元放電的影響,探討低頻電刺激PPN治療PD的作用機製。方法30隻SD大鼠隨機分為對照組和PD組各15隻。大鼠腦右側黑質緻密部註入6-羥基多巴胺建立PD模型;採用細胞外記錄方法,利用7管玻璃微電極記錄觀察低頻電刺激、微電泳穀氨痠(Glu)及其受體阻斷劑MK-801、γ-氨基丁痠(GABA)及其受體阻斷劑荷包牡丹堿(BIC)對大鼠GPi神經元放電頻率的影響。結果低頻電刺激PPN,對照組及PD組大鼠GPi神經元反應均以抑製為主,且平均放電頻率均較刺激前降低(P<0.01);微電泳Glu和BIC對神經元有興奮作用,而微電泳MK-801和GABA對神經元有抑製作用。在微電泳BIC的興奮作用的基礎上低頻電刺激PPN使神經元放電頻率明顯降低,而在微電泳MK-801抑製作用的基礎上低頻刺激PPN使神經元放電頻率進一步降低。結論低頻電刺激PPN可抑製GPi神經元活動,可能是通過調節投射到GPi神經元的Glu和GABA神經通路實現的。
목적:통과관찰저빈전자격파금삼병(PD)모형대서각교핵(PPN)대창백구내측부(GPi)신경원방전적영향,탐토저빈전자격PPN치료PD적작용궤제。방법30지SD대서수궤분위대조조화PD조각15지。대서뇌우측흑질치밀부주입6-간기다파알건립PD모형;채용세포외기록방법,이용7관파리미전겁기록관찰저빈전자격、미전영곡안산(Glu)급기수체조단제MK-801、γ-안기정산(GABA)급기수체조단제하포모단감(BIC)대대서GPi신경원방전빈솔적영향。결과저빈전자격PPN,대조조급PD조대서GPi신경원반응균이억제위주,차평균방전빈솔균교자격전강저(P<0.01);미전영Glu화BIC대신경원유흥강작용,이미전영MK-801화GABA대신경원유억제작용。재미전영BIC적흥강작용적기출상저빈전자격PPN사신경원방전빈솔명현강저,이재미전영MK-801억제작용적기출상저빈자격PPN사신경원방전빈솔진일보강저。결론저빈전자격PPN가억제GPi신경원활동,가능시통과조절투사도GPi신경원적Glu화GABA신경통로실현적。
Objective To explore the mechanism of the low-frequency electrical stimulate on pedunculopontine nu-cleus to treat the Parkinson (PD) through observinge the low-frequency electrical stimulation of Pedunculopontine Nucleus (PPN) in PD rat model and the effects of neurotransmitters (GPi) neurons discharge in the medial part of the globus pallidus. Methods Thirty SD rats were randomly assigned to the control group and the PD model group, with 15 in each group. PD model was established through injecting 6-OHDA into Substantia nigra compact (SNc) of black rat. Effect of low frequency electrical stimulation, micro-electrophoresis glutamate (Glu) and its receptor blocking breaking agent MK-801,γ-aminobu-tyric acid (GABA) and its receptor antagonist bicuculline (BIC) on discharge of rat neuron GPi was examined using extracel-lular unit recording methods through seven glass microelectrode recording. Results When stimulated by low frequency electrical stimulation of PPN, reactions from the control group and neuronal response GPi in PD rats were inhibited. The aver-age discharge frequency was reduced compared to pre-stimulation (P < 0.01). Micro-electrophoresis and BIC Glu excite neurons while microiontophoresis MK-801 and GABA restrain neurons. In the background of micro-electrophoresis BIC’s excitatory effects on neuron, low-frequency electrical stimulation on PPN reduced neuronal firing frequency. And in the background of inhibition effect of micro-electrophoresis MK-801, low-frequency stimulation PPN further restrain neuronal discharge frequency. Conclusion Low frequency electrical stimulation inhibits GPi PPN neuronal activity probably though regulating neurons projecting to the Glu and GABA nerve pathways in GPi neuron.