Double Labeling Immulloelectron Microscopic Study on the Synaptic Connections between Glutamic Acid Neurons and GABA Neurons in the Hippocampus of Rats

The pathogenesis of epilepsy is a very complicated process, In which neurotransmltters play important roles. The hippocamplls is a frequently attacked site and an ideal model tissue for epilepsy' l]. In general, the seizure results from the imbalance of excitation and inhibition, i. e., increased effect of excltatory neurotransmltters ordecreased effect of inhlbitory neurotransrnlttersL =' ']. However, there was no nlorphologlcal, eel)eclally at the ultrastructural level, evidenceic identify …     

隔区通过GABA_A抑制缰核活动产生电针镇痛作用

通过多管微电泳记录大鼠缰核单位放电和测定痛阐的方法观察到：ＧＡＢＡＡ可完全抑制缰植的自发放电；电刺激隔区强力抑制缰核的自发放电，Ｂｉｏｕｏｕｌｌｉｎｅ则使该作用减弱；双侧缰核内微量注射ＧＡＢＡ使痛阐明显升高，Ｂｉｃｕｃｕｌｌｉｎｅ则相反并拮抗电针镇痛效应。提示隔区通过ＧＡＢＡ抑制缰核活动产生电针镇痛作用     

Double labeling immunoelectron microscopic study on the synaptic connections between glutamic acid neurons and GABA neurons in the hippocampus of rats

Summary In order to explore the roles of different neurotransmitters in epileptic pathogenesis, the synaptic connections between glutamic acid (Glu) neurons and GABA neurons in normal rat hippocampus were studied by pre-embedding double labeling immunoelectron microscopy. The GABA immunoreaction was first demonstrated by chromogen DAB, then the Glu immunoreaction was demonstrated by molybdic acid-TMB method. After being stabilized by DAB-cobalt chloride, the sections were processed for electron microscopic embedding. Under electron microscope, there were many Glu immunoreaction-positive neurons in the pyramidal layer of hippocampal CA₁ area and some GABA immunoreaction-positive neurons with pyramidal or polygonal perikarya in the pyramidal, polymorphic and radiant layer of CA₁ area. There were also symmetric dendro-axonic synapses formed by GABA-positive dendrites and Glu-positive axons in the polymorphic layer and symmetric axo-dendritic synapses formed by GABA-positive axons and Glu-positive dendrites in the radiant layer. In addition, there were symmetric autoregulatory axo-dendritic synapses between Glu-positive axons and dendrites and autoregulatory axo-axonic synapses (both symmetric and asymmetric) between GABA-positive axons. Above mentioned results, for the first time, showed that there were complex synaptic regulatory relationships between excitatory Glu neurons and inhibitory GABA neurons in the hippocampal CA₁ area, thereby, providing ultrastructural evidence for different neurotransmitters participating in epileptic pathogenesis. This project was supported by a grant from the National Nature Scientific Foundation of China (No. 39330210).     

颅脑创伤后海马区钾-氯协同转运蛋白-2、γ-氨基丁酸的表达变化及亚低温治疗对其影响

目的探讨脑创伤(TBI)大鼠钾-氯协同转运蛋白2(KCC2)和γ-氨基丁酸(GABA)的表达变化及亚低温治疗对其影响。方法将30只Wistar大鼠随机分为对照组(C组)、创伤组(TBI组,给予液压冲击,不做处理)和治疗组(T组,液压冲击后接受亚低温治疗,32℃),亚低温干预在创伤后即刻给予32℃低温处理持续6 h。高效液相色谱法测定GABA水平,酶联免疫吸附试验检测各组大鼠血清KCC2水平;反转录-聚合酶链反应、Western blotting检测各组大鼠脑组织中KCC2 mRNA和蛋白的表达。结果与C组比较,T组、TBI组大鼠血清KCC2水平、脑组织KCC2蛋白及mRNA表达均显著降低(P<0.05);T组大鼠血清KCC2水平较TBI组显著增高,差异有统计学意义(P<0.05);GABA变化趋势与KCC2相反。结论 KCC2在大鼠脑创伤过程中表达降低,亚低温进行干预可上调KCC2的表达、下调GABA表达。     

地黄寡糖对糖尿病大鼠空间学习记忆的影响

目的研究地黄寡糖对糖尿病大鼠空间学习记忆的影响及其机制。方法采用链脲佐菌素制备大鼠糖尿病模型,随机分为正常对照组、正常用药组（500 mg/kg）、糖尿病模型组、低剂量和高剂量地黄寡糖治疗组（100 mg/kg、500 mg/kg）;定期检测动物体重及血糖;11周后进行Morris水迷宫实验测定大鼠学习记忆能力,随后取海马组织,测定谷氨酸和γ-氨基丁酸含量。结果模型组、低剂量治疗组和高剂量治疗组与对照组相比,体重都明显减轻,血糖也明显升高,海马组织中谷氨酸水平分别提高了30.8%（P〈0.05）,32.5%（P〈0.01）和29.9%;同时模型组比对照组逃避潜伏期明显延长,在原平台象限游泳时间占总游泳时间的百分比明显降低;低剂量治疗组和高剂量治疗组与模型组相比,逃避潜伏期明显缩短,在原平台象限的游泳时间占总游泳时间的百分比明显增加,并且γ-氨基丁酸含量分别高出模型组13.7%和14.8%;正常用药组和对照组相比,γ-氨基丁酸含量明显升高。结论糖尿病大鼠空间学习记忆能力下降,地黄寡糖对其学习记忆能力具有一定的改善作用,这可能与其提高海马组织中γ-氨基丁酸的相对水平,防止高水平谷氨酸引起的神经元过度兴奋有关。