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背景:羧乙基锗倍半氧化物(carboxyethygermaniumsesquioxide,Ge-132)是近30年研究较多的具有多种生物活性的有机锗化合物,临床试验性用于老年痴呆症和及其他多种疾病的预防和治疗。但有机锗对神经系统作用环节及机制尚未见文献报道较少。目的:探索Ge-132对大鼠颈上神经节细胞及烟碱传递过程的影响。设计:非随机自身对照实验性研究。地点和材料:实验在广西医科大学实验中心神经药理学实验室完成。材料:成年Wistar大鼠30只,雌雄兼用。干预:大鼠急性处死后,迅速将颈上神经节连同节前神经离体,用950mL/LO2和50mL/LCO2混合气饱和的,pH为7.4±0.05的克氏溶液,恒温(35±0.5)℃持续灌流。用内充灌3M-KCl溶液的玻璃微电极穿刺离体颈上神经节神经元进行细胞内记录。所有的药物均用Kreb液中配成相应浓度直接灌流神经节。主要观察指标:快兴奋性突触后电位(FEPSP)。结果:①Ge-132在1×10-4mol/L或更高浓度,可逆地抑制刺激节前神经引起的FEPSP的幅度,并可使动作电位发放频率减少。②对乙酰胆碱(ACh)引起的膜除极反应无显著的影响。③对细胞膜被动膜性质无明显的影响。结论:Ge-132对烟碱传递的抑制作用可能是其使突触前ACh释放减少所至。
BACKGROUND: Carboxyethylgermanium sesquioxide (Ge-132) is a kind of organogermanium compound with many biological activity that has been studied for more than 30 years. It is used clinically in Alzheimer’s disease and other diseases Prevention and treatment. But organic germanium on the nervous system and its mechanisms have not been reported in the literature reported less. Objective: To explore the effect of Ge-132 on the rat superior cervical ganglion cells and nicotine transmission. Design: Non-randomized self-controlled experimental study. Location and Materials: Experiments were performed at the Neuropharmacology Laboratory, Guangxi Medical University Experimental Center. MATERIALS: Thirty adult Wistar rats were used both sexes. Intervention: Immediately after the rats were sacrificed, the superior cervical ganglion and the preganglionic nerve were exfoliated rapidly. The rats were fixed in a Krebs solution (pH 7.4 ± 0.05) saturated with 950 mL / L O2 and 50 mL / ℃ continued perfusion. Intrathoracic ganglion neurons were disseminated intracellularly using a glass microelectrode filled with 3M-KCl solution. All drugs were Kreb solution dubbed the corresponding concentration of direct perfusion ganglia. MAIN OUTCOME MEASURES: Fast excitatory postsynaptic potential (FEPSP). Results: ①Ge-132 reversibly inhibited the amplitude of FEPSP induced by stimulation of preganglionic nerve at a concentration of 1 × 10-4mol / L or higher, and decreased the release frequency of action potential. ② Acetylcholine (ACh) induced membrane depolarization had no significant effect. ③ no significant impact on the nature of the membrane passive membrane. CONCLUSIONS: The inhibitory effect of Ge-132 on nicotinic transmission may be due to its reduced presynaptic ACh release.