陈蕾
主要从事神经生理领域的研究。
个性化签名
- 姓名:陈蕾
- 目前身份:
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学术头衔:
博士生导师
- 职称:-
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学科领域:
生理学
- 研究兴趣:主要从事神经生理领域的研究。
陈蕾,女,1963年出生。1986年获青岛医学院医学学士学位,并作为优秀毕业生被免试推荐为青岛医学院生理学专业硕士研究生。1989年获青岛医学院硕士学位后留校任教。2004年获香港中文大学医学院生理专业博士学位。2003年于英国牛津大学药理系进修学习。2005年于香港中文大学从事博士后研究。现任青岛大学医学院生理教研室主任,教授,博士生导师,山东省“十一五”生理学重点强化建设学科负责人。
主要从事神经生理领域的研究。运用脑片膜片钳及受体免疫电镜等实验技术,从离体、在体,形态、功能,细胞、整体等多个层次,系统探讨了基底神经节突触传递及其与神经源性疾病的关系。
作为课题主要完成人参与多项国家及省厅级课题的研究,获省级科技进步奖3项、市厅级科技进步奖6项。目前承担国家自然科学基金2项,山东省自然科学基金和山东省卫生厅课题各1项。共发表研究论文50余篇,其中20篇为SCI收录文章。承担研究生神经生物学、细胞信息与调控、电生理学理论与技术以及本科生生理学双语教学任务,多次被评为课堂教学效果优秀教师。2000年获青岛市第二届青年科技奖,2005年获准为第二批山东省医学卫生中青年重点科技人才。
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成果数
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陈蕾, L. CHEN, a, b S. C. Y. CHANa and W. H. YUNGa*
,-0001,():
-1年11月30日
GABA is the major neurotransmitter used in the globus pallidus and there is evidence that GABAB receptors exist in this nucleus. Here we show that unilateral microinjection of baclofen, a GABAB receptor agonist, induced ipsilateral turning in Sprague^Dawley rats. This e
baclofen,, CGP55845A,, heteroreceptor.,
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【期刊论文】Electrophysiological and behavioral effects of zolpidem in rat globus pallidus
陈蕾, Lei Chen, a C. Savio Chan, b and Wing-Ho Yunga, *
Experimental Neurology 186(2004)212-220,-0001,():
-1年11月30日
The globus pallidus is believed to play a critical role in the normal function of the basal ganglia, and abnormal activity of its neurons may underlie some basal ganglia motor symptoms. A high density of benzodiazepine binding sites on GABAA receptors has been reported in the rat globus pallidus. The present study investigates the effect of activating the benzodiazepine site by the agonist zolpidem. In in vitro slices, 100 nM of zolpidem significantly prolonged the half decay time of both miniature and spontaneous inhibitory postsynaptic currents by 30.1
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【期刊论文】Subcellular Localization of GABAB Receptor Subunits in Rat Globus Pallidus
陈蕾, LEI CHEN, , JUSTIN BOYES, WING-HO YUNG, AND J. PAUL BOLAM*
THE JOURNAL OF COMPARATIVE NEUROLOGY 474: 340-352 (2004),-0001,():
-1年11月30日
The inhibitory amino acid-aminobutyric acid (GABA) is the major neurotransmitter in the globus pallidus. Although electrophysiological studies have indicated that functional GABAB receptor subunits and their spatial relationship to glutamatergic and GABAergic synapses are un-known. Here, we use pre-embedding immunogold labeling to study the subcellular localiza-tion of GABAB receptor subunits, GABAB1 and GABAB2, in globus pallidus neurons and identified populations of afferent erminals. Immunolabeling for GABAB1 and GABAB2 was observed throughout the globus pallidus, with GABAB1 more strongly expressed in perikarya and GABAB2 mainly expressed in the neuropil. Electron microscopic analysis revealed that the majority of GABAB1 labeling was localized within the ytoplasm, whereas most of GABAB2 labeling was associated with the plasma membrane. At the subcellular level, both the GABAB1 and GABAB2 immunogold labeling was found at perisynaptic sites of both pre- and postsynaptic specializations. Double immu-nolabeling, using the vesicular glutamate transporter 2 (VGLUT2), revealed the glutama-tergic nature of most immunogold-labeled asymmetric synapses. At symmetric, putative GABAergic, synapses, including those formed by anterogradely labeled striatopallidal terminals, GABAB1 and GABAB2 immunogold labeling was found in the main body of both pre- and postsynaptic specializations. These results demonstrate the existence of resynaptic GABAB auto- and heteroreceptors and postsynaptic GABAB receptors, which may be involved in odulating synaptic transmission in the globus pallidus. J. Comp. Neurol. 474:340–352, 2004. © 2004 Wiley-Liss, Inc.
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【期刊论文】NEUROTENSIN DEPOLARIZES GLOBUS PALLIDUS NEURONS IN RATS VIA NEUROTENSIN TYPE-1 RECEPTOR
陈蕾, L. CHEN, a K. K. L. YUNGb AND W. H. YUNGa*
Neuroscience 125(2004)853-859,-0001,():
-1年11月30日
The globus pallidus is a major component in the indirect pathway of the basal ganglia. There is evidence that neurotensin receptors exist in this nucleus. To determine the electrophysiological effects of neurotensin on pallidal neurons, whole-cell patch-clamp recordings were performed in the acutely prepared brain slices. Under current-clamp recordings, neurotensin at 1M depolarized pallidal neurons. Voltage-clamp recordings also showed an inward current induced by neurotensin. The depolarizing effect of neurotensin could be mimicked by the C-terminal fragment, neurotensin (8-13), but not by the N-terminal fragment, neurotensin (1-8). Both SR 142948A, a non-selective neurotensin receptor type-1 and type-2 antagonist, and SR 48692, a selective type-1 receptor antagonist, blocked the depolarizing effect of neurotensin, and which themselves had no effect on membrane potential. Thus, neurotensin type-1 receptors appear to mediate the effect of neurotensin. The depolarization evoked by neurotensin persisted in the presence of tetrodotoxin, ionotropic and metabotropic lutamate and GABA receptor antagonists, indicating that neurotensin excited the pallidal neurons by activating the receptor expressed on the neurons recorded. Current-voltage relationship revealed that both the suppression of a potassium conductance and the activation of a cationic conductance are involved in the neurotensininduced depolarization. Based on the action of neurotensin in the globus pallidus we hypothesize that alterations of the striatopallidal neurotensin system contribute to symptoms of basal ganglia motor disorders.
neurotensin,, SR48692,, SR142948A,, globus pallidus.,
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