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中国神经科学学会第十二届全国学术会议

作者： Li-jie Zhan Bing-xue Li Dan Wang De-lai Qiu Yan Lan cellular Function Research Center Yanbian University Department of Physiology and Pathophysiology College of Medicine Yanbian University Department of pharmacology College of Medicine Yanbian University Key Laboratory of Natural Resource of the Changbai Mountain and Functional Molecular of the Ministry of Education Yanbian University

Background: It has been reported that the mechanisms of morphine addiction is the homeostasis dysregulation of brain. The cerebellum is involved in control of motor coordination and receives sensory inputs to execute complex motor tasks. Increasing evidence has involved that addiction is related to a disruption in cerebellar processing and connectivity with other brain regions. However, the changes of information processing in cerebellum in morphine addiction is unknown. In present research, our aim is to observe the effects of morphine dependence and withdrawal on sensory information processing in cerebellar granule cell layer in vivo in mice. Methods and Main Results: Forty male KM mice were randomly divided into four groups（n=10）: the morphine dependence group, morphine withdraw 1 day group, morphine withdrawal 7 days group, and the saline control group. The mice in dependence group and withdrawal group were administered with morphine by subcutaneous injection through the method of "increasing addiction for 7 days", and the saline group were injected saline. Mice administered morphine exhibited opioid-like responses including Straub tail and hyperlocomotion in behavior. Electrophysiological methods were used in our research to record the field potential of granule cell layer（GCL）. Air-puff stimulation of the ipsilateral whisker-pad evoked stimulus-on（N1） and stimulus-off responses（N2） in GCL of cerebellar Crus II. The amplitude of N1 and N2 in dependence group, withdrawal 1 day group and withdrawal 7 day group are obviously decreased compared with control group（p＜0.05）, and withdrawal 1 day group shows a marked drop compared with dependence group and withdrawal 7 day group（p＜0.05）. The onset latency of the sensory stimulationevoked responses has no change. Conclusion: These results indicate that morphine dependence and withdrawal affect the homeostatic regulation of sensory information processing in cerebellar granule cell layer.

关键词： Morphine dependence Morphine withdrawal cerebellar granule cell Mice Sensory stimulation

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Inhibition of mitochondria responsible for the anti-apoptotic effects of melatonin during ischemia-reperfusion

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2006年第2期7卷 142-147页

作者：韩义香章圣辉王西明吴建波 Institute of Medical Science the First Affiliated Hospital Wenzhou Medical College Wenzhou 32500 China Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 China

Objective： To investigate a possible mechanism responsible for anti-apoptotic effects of melatonin and provide theoretical evidences for clinical therapy. Methods： lschemia-reperfusion mediated neuronal cell injury model was constructed in cerebellar granule neurons （CGNs） by deprivation of glucose, serum and oxygen in media. After ischemia, melatonin was added to the test groups to reach differential concentration during reperfusion. DNA fragmentation, mitochondrial transmembrane potential, mitochondrial cytochrome c release and caspase-3 activity were observed after subjecting cerebellar granule neurons to oxygen-glucose deprivation （OGD）. Results： The results showed that OGD induced typical cell apoptosis change, DNA ladder and apoptosis-related alterations in mitochondrial functions including depression of mitochondrial transmembrane potential （its maximal protection ratio was 73.26%） and release of cytochrome c （its maximal inhibition ratio was 42.52%） and the subsequent activation of caspase-3 （its maximal protection ratio was 59.32%） in cytoplasm. Melatonin reduced DNA damage and inhibited release of mitochondrial cytochrome c and activation of caspase-3. Melatonin can strongly prevent the OGD-induced loss of the mitochondria membrane potential. Conclusion： Our findings suggested that the direct inhibition of mitochondrial pathway might essentially contribute to its anti-apoptotic effects in neuronal ischemia-reperfiusion.

关键词： cerebellar granule cell Ischemia-reperfusion Cytochrome c Melatonin

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Effects of cholesterol on neuronal apoptosis via modulation of IK channels

Effects of cholesterol on neuronal apoptosis via modulation ...

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中国神经科学学会第四次会员代表大会暨第八届全国学术会议

作者： Meng-Hua ZHOU,Song JIAO,Yan-Ai MEI~* Institute of Brain Science,School of Life Sciences and State Key Laboratory of Medical Neurobiology,Fudan University, Shanghai 200433,China

The lipid rafts on the cell membrane which are associated with various diseases,are very important structures for modulating intracellular signal transduction and ion channel *** previous results have revealed that two types of K channels in the rat granule neurons(GC) were up-regulated during neuron apoptosis induced by a medium treatment of low potassium without serum(LK-S).However,no evidence has demonstrated whether this change involves the lipid rafts of neuron *** the present study,we observed that the change in the lipid raft component using the cholesterol or methyl-β-cyclodextrin(MβCD) modulated the cerebellar granule cells’ sensitivity to the LK-S *** the cholesterol(15μM) in the bath solution significantly reduced the viable rate of neurons under the LK-S medium control from(52.7±6.00)%to(29.3±5.20)%.On the other hand,depleting membrane cholesterol by MβCD(500μM) could increase the viable rate in the same treatment condition to(83.1±5.60)%.Neither the enhancement nor the depletion of cholesterol induced neural apoptosis in normal culture *** our previous studies have indicated,IK channels are involved in apoptosis,and Kv2.1channel is the main component of IK channels in *** therefore examined whether cholesterol-induced neural apoptosis occurred via the modulation of IK ***-cell current recording revealed that the application of cholesterol(15μM)) drastically increased the IK current[current amplitude increased from(673.1±32.8) pA to(957.1±42.9) pA].However,cholesterol depletion by MβCD(500μM) decreased the IK current under LK-S treatment. Applying cholesterol or depleting membrane cholesterol does not modify the kinetic properties of the IK current. Furthermore,addition of cholesterol to the culture medium promoted the expression and induced the clustering of the Kv2.1α-subunit on cell membranes,as detected by western blotting and immunostaining *** results suggest that these changes in the compon

关键词： cholesterol neuronal apoptosis Kv2.1 IK cerebellar granule cell

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Antioxidant activity of new natural compound Vam-3

Antioxidant activity of new natural compound Vam-3

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2002全国青年药理学英文学术会议

作者： WANG Qing-li LIU Geng-taoInstitute of Materia Medcia, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China

AIM: Vam-3, a dimer of resveratrol, is a new natural compound isolated from Vitis amurensis. Resveratrol is produced by some spermatophytes such as grapevines in response to injury and fungal attack. Resveratrol possesses potent antioxidant activity exerted by its 3 phenolic hydroxyl groups in its structure. It is quite possible that Vam-3 also has antioxidative activity. The present study investigated the antioxidant effect of Vam-3. METHODS: Lipid peroxidation of rat liver microsomes was induced by Fe-cystine (Cys) and VitC-ADP-Fe, two reactive oxygen species (ROS) generating systems. The effect of

关键词： Antioxidant Oxidative DNA damage cerebellar granule cell

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