海马谷断裂北西盘金矿化蚀变带的发现及地质意义

戈塘金矿床是黔西南地区发现最早的大型金矿床之一,其金矿体均分布于区域性海马谷断裂南东盘。经近30年的断续找矿工作,海马谷断裂北西盘找矿方向及前景却依然不清。在新近的矿产地质调查工作中,在海马谷断裂北西盘,通过地电化学测量提取Au元素峰值为179.0×10^(-9),经异常查证发现荞地坡金矿化蚀变带,该金矿化蚀变带受控于下三叠统嘉陵江组一段与二段岩性突变界面,呈似层状产出,沿走向延伸1.2 km,厚0.8~2.0 m,含金品位为0.50×10^(-6)~0.82×10^(-6)。其发现过程折射出地电化学测量的引入对戈塘地区金矿找矿起到积极促进作用;也拓展了该地区找矿空间,分析认为在海马谷断裂北西盘深部有利岩性组合段与北东向构造叠加部位具有较好的金矿找矿前景。

贵州海马谷地区金矿矿床特征及成矿模式

本文对海马谷地区金矿进行调查,在贵州安龙海马谷发现北东向陡倾角断层控制金矿体,其围岩为二叠系茅口组生物灰岩,矿石为硅化灰岩角砾岩。根据本次调查及收集已有勘查研究成果,建立了该区的成矿模式,认为该区北东向陡倾角断层是下一步该区重要的找矿目标。

Environmental cues associated with morphine modulate release of glutamate and γ-aminobutyric acid in ventral subiculum

Objective To investigate whether environmental cues associated with different properties of morphine could regulate the extracellular levels of glutamate and y-aminobutyric acid （GABA） in the hippocampal ventral subiculum, which play a critical role in the reinstatement of drug-seeking behavior induced by environmental cues. Methods Conditioning place preference （CPP） and conditioning place aversion （CPA） models were used to establish environment associated with rewarding and aversive properties of morphine respectively. Microdialysis and high performance liquid chromatography were used to measure the extracelluar level of glutamate and GABA in the ventral subiculum under these environmental cues. Results Exposure to the environmental cues associated with rewarding properties of morphine resulted in a decrease （approximately 11%） of extracellular level of GABA in ventral subiculum, and exposure to the environmental cues associated with aversive properties of morphine resulted in an increase （approximately 230%） of extracellular level of glutamate in ventral subiculum. Conclusion Environmental cues associated with different properties of morphine modulate the release of distinct neurotransmitters in the hippocampal ventral subiculum possibly through different neural circuit.

Glutamine synthetase activity and glutamate uptake in hippocampus and frontal cortex in portal hypertensive rats

AIM: To study glutamine synthetase (GS) activity and glutamate uptake in the hippocampus and frontal cortex (FC) from rats with prehepatic portal vein hypertension. METHODS: Male Wistar rats were divided into shamoperated group and a portal hypertension (PH) group with a regulated stricture of the portal vein. Animals were sacrificed by decapitation 14 d after portal vein stricture. GS activity was determined in the hippocampus and FC. Specific uptake of radiolabeled L-glutamate was studied using synaptosome-enriched fractions that were freshly prepared from both brain areas. RESULTS: We observed that the activity of GS increased in the hippocampus of PH rats, as compared to control animals, and decreased in the FC. A significant decrease in glutamate uptake was found in both brain areas, and was more marked in the hippocampus. The decrease in glutamate uptake might have been caused by a deficient transport function, signif icantly and persistent increase in this excitatory neurotransmitter activity. CONCLUSION: The presence of moderate ammonia blood levels may add to the toxicity of excitotoxic glutamate in the brain, which causes alterations in brain function. Portal vein stricture that causes portal hypertension modif ies the normal function in some brain regions.

Effect of neuronal excitotoxicity on Munc18-1 distribution in nuclei of rat hippocampal neuron and primary cultured neuron

Objective Muncl8-1 has an important role in neurotransmitter release, and controls every step in the exocy- totic pathway in the central nervous system. In the present study, whether epileptic seizure causes a change of Muncl8 localization in neuronal nuclei was analyzed. Methods Epilepsy models were established by injection of kainic acid （KA） solution into hippocampus of Sprague-Dawley （SD） rats or intraperitoneal injection of KA in Kunming mice. The hippocampal neurons were prepared from embryonic day 18 SD rats, and cultured in neurobasal medium, followed by treatment with glutamate for 3 h. Neuronal and glial nuclei of hippocampus were separated by sucrose density gradient centrifugation. The nucleus-enriched fractions were stained with 0.1% Cresyl Violet for morphological assay. Immuno- chemistry and immunoelectron microscopy with anti-Muncl 8-1 antibody were used to determine the nuclear locatization of Munc 18-1. Immunoblotting was used to detect the protein level of Munc 18-1. Results The localization of Munc 18-1 in nucleus of rat hippocampal neuron was confirmed by immunochemistry, immunoelectron microscopy, and immunob- lotting detection of neuronal nucleus fraction. In animals receiving intrahippocampal or intraperitoneal injection of KA, immunostaining revealed that the expression of Muncl 8-1 decreased in pyramidal cell layer of CA regions, as well as in hilus and granular cell layer of dentate gyrus in hippocampus. Moreover, immunoblotting analysis showed that the expres- sion level of Muncl 8-1 in nucleus fraction of hippocampus significantly decreased in KA-treated animals. The relation- ship between the change of Muncl8-1 expression in neuronal nuclei and neuronal over-activation was also tested in pri- mary cultured neurons. After treatment with 50 ~tmol/L glutamate acid for 3 h, Muncl8-1 level was decreased in nucleus fraction and increased in cytoplasmic fraction of primary cultured neurons. Conclusion These results suggest that excit- atory stimulation can induce the distribution change of Munc 18-1 in neuron, which may subsequently modulate neuronal functions in brain.