谢俊霞
主要从事中枢多巴胺能神经系统与帕金森病(PD)发病相关因素在PD发病机制中的作用及防治对策研究。
个性化签名
- 姓名:谢俊霞
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学术头衔:
博士生导师
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学科领域:
神经生物学
- 研究兴趣:主要从事中枢多巴胺能神经系统与帕金森病(PD)发病相关因素在PD发病机制中的作用及防治对策研究。
谢俊霞,女,1956年9月生,博士,生理学教授、博士生导师,任青岛大学副校长。山东省生理学“十五”强化建设重点学科负责人,山东省神经科学研究中心主任,兼任“中国生理学会”及“中国神经科学学会”常务理事,山东省生理学会副理事长,山东省医学会副会长,山东省六届科协委员,山东省七大、八大党代表,青岛市九届、十届政协委员。担任《生理学报》、《中国神经科学杂志》编委和《青岛大学医学院学报》主编。
主要从事中枢多巴胺能神经系统与帕金森病(PD)发病相关因素在PD发病机制中的作用及防治对策研究,逐渐形成并奠定了本研究方向的特色,受到国内外同行专家的公认。1997年以来主持完成国家自然基金课题1项,山东省自然科学基金项目3项,卫生部课题1项和省教育厅重点项目1项。其科研成果获厅局级以上奖励9项,其中分别获首届山东省和青岛市2002、2003年度科学技术奖(自然科学奖)二等奖各1项,获山东省科技进步奖3项,青岛市科技创新奖1项,山东省教育厅优秀科技成果奖3项。
目前主持研究课题8项,其中国家自然科学基金课题2项,省科委课题1项,省教育厅重点项目1项,市科委课题2项,香港理工大学合作课题2项。在国际、国内专业学术期刊发表研究论文50余篇,其中SCI收录11篇,CA收录9篇。出席国际学术会议交流研究结果17次。1992-1996年间三次赴德国慕尼黑大学工作,进行合作研究。培养硕士毕业生11名,博士毕业生2名,在读博士生6名,硕博连读生2名,硕士生6名。指导的研究生2人获山东省优秀硕士论文奖;2人获中国生理学会张锡钧基金优秀论文奖。1999年被评为青岛市第二批工程技术、学术带头人;2000年被评为山东省优秀科技工作者并被授予青岛市“三八红旗手”;2002年被评为青岛市“巾帼科技创新英才”并被授予山东省和青岛市“三八红旗手”;2003年被授予青岛市专业技术拔尖人才。
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190
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成果数
5
谢俊霞, Bin Liu and Junxia Xie
Journal of Neurochemistry 90(2004) 654-658,-0001,():
-1年11月30日
In addition to the dopaminergic neurons in the nigrostriatal system, the properties of dopaminergic neurons in the mesolimbic system, such as the amygdala, are also of interest and importance because of their specific neuromodulatory effects in the pathophysiology of Parkinson’s disease (PD). Using the fast cyclic voltammetry (FCV) technique, we present evidence to indicate that electrically-evoked dopamine (DA) release from the amygdala, especially the central amygdaloid nucleus (CAN), of ovariectomized (OVX) female rats was significantly enhanced with increasing doses of estradiol benzoate (EB; 30, 50 and 100 μg/kg). Impaired DA release from the amygdala of an OVX rat PD model can also be increased by EB treatment (50μg/kg) to a level similar to that of controls. The well established neuroprotective effects of estrogen may be beneficial for reducing the dysfunction of dopaminergic neurons in mesolimbic structures of rat PD models and PD patients.
amygdala, dopamine, estrogen, Parkinson', s disease, rats
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【期刊论文】C31 enhances voltage-gated calcium channel currents in undifferentiated PC12 cells
谢俊霞, Ze-Gang Ma, Jun Wang, Hong Jiang, Jun-Xia Xie∗, Lei Chen
Neuroscience Letters 382(2005) 102-105,-0001,():
-1年11月30日
C31, consisting of 31 amino acid residues, is generated from the carboxyl terminal fragments (CTFs) of amyloid precursor protein (APP).It has been shown that C31 causes apoptosis in neurons and is present in brains of Alzheimer disease (AD) patients. Using whole-cell patch clamp techniques, we investigated effects of C31 on voltage-gated calcium channel (VGCC) currents and the protective effects of β-estradiol on PC12 cells. The results demonstrated that C31 induced a significant increase of the VGCC currents in PC12 cells, which was blocked by β-estradiol. These results suggest that modulation of intracellular calcium levels by VGCC may in part be involved in C31 induced neuronal death associated with AD.
Alzheimer', s disease, C31, Voltage-gated calcium channel
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谢俊霞, Xie Junxia, a, * Jiang Hong, b Chen Wenfang, b and Qian Zhong Ming b, *
Experimental Neurology 182(2003) 483-489,-0001,():
-1年11月30日
The effects of intranigral iron injection on dopamine (DA) release and content in the caudate putamen(CPu)and their relationship to DA-related behavioral response were investigated in rats. Different concentrations of FeCl3 (10, 20, and 40μg) and saline were injected separately into the left substantia nigra. In some experiments, rats were pretreated with desferrioxamine or saline before iron injection. After 3 weeks, changes in behavioral response, DA release, and DA content in the CPu were determined. In all iron injection groups (10, 20, and 40μg), DA content in the lesioned side of the brain was significantly decreased, showing a significant linear correlation (R2 0.981, P<0.01), and DA turnover ratio significantly increased (both P<0.01, 0.01and 0.001 vs unlesioned sides, respectively). However, injection dosages of 10 or 20μg of iron did not lead to significant changes in DA release in the CPu or in behavioral response. At the 40-μg dosage, it was found that DA release in the lesioned side and rearing activity both were significantly reduced (all P<0.01 vs unlesioned side or control) and apomorphine-induced rotation was observed. Pretreatment with desferrioxamine significantly inhibited the effect of iron on DA release and content. These results demonstrate that iron injection can damage dopaminergic neurons and suggest that DA release, rather than DA content, in the CPu is associated with DA-related behavioral changes in this PD model.
Parkinson', s disease, Intranigral iron injection, Dopamine release and content, Nigrostriatal dopaminergic neurons, Desferrioxamine
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谢俊霞, JUN-XIA XIE, MING TANG and CHUNYI ZHANG*
Prog. Neuro-Pstychopharmacol. & Biol, Psychiat, 2001, Vol.25, pp.427-434,-0001,():
-1年11月30日
XIE JUN-XIA, MING TANG and CHUNYI ZHANG: Effect of cholecystokinin-8 mieroinjeetion into ventral tegmental area on dopamine release in nucleus accumbens of rats: An in vivo voltammclric study. Prog. Neuro-Psyehopharmaeol.& Biol.Psychiat.2001, 25 pp.427-434.
cholecystokinin, dopamine, electrical stimulation, medial forebraln bundle, nucleus accumbens, ventral tegmental area, voltammetry
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【期刊论文】Effects of isatin on rotational behavior and DA levels in caudate putamen in Parkinsonian rats
谢俊霞, Yu Zhou a, b, Zhi-Qi Zhao b, Jun-Xia Xie a, *
Brain Research 917(2001) 127-132,-0001,():
-1年11月30日
Isatin was a potent endogenous monoamine oxidase (MAO) inhibitor that is more active against MAO-B than MAO-A. The acute effects of isatin on apomorphine (APO)-induced rotations were evaluated in Parkinsonian rats induced by 6-hydroxydopamine (6-OHDA) lesion. Furthermore, the effects of isatin on DA release in caudate putamen (CPu) of model and normal rats were monitored using fast cyclic voltammetry (FCV). The contents of monoamine transmitters and their metabolites in CPu of model and normal rats were also analyzed by high performance liquid chromatography with electrochemical detection after administration of isatin. Here we show that isatin (100mg/kg,i.p.)apparently inhibited APO-induced rotations of Parkinsonian rats to 39.1±3.7% of the control (n=12), while it had no apparent effects on electrical stimuli-induced DA release either in normal rats or in model rats. In addition, the content of 5-hydroxytryptamine but not DA was increased in both normal rats and model rats after isatin (100 mg/kg,i.p.) was administered (P<0.01, n=6). The content of 5-hydroxyindole acetic acid was not changed. These results suggest that isatin cannot increase DA levels in rat CPu. Therefore, the effects of isatin on APO-induced rotations of our Parkinsonian rats could not attribute to its inhibition of DA catabolism as a MAO inhibitor.
Isatin, Dopamine, Rotation, Parkinsonian rat, Fastcyclic voltammetry, High-performance liquid chromatography with electrochemical detection
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