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Chinese Science Bulletin 1991年第9期36卷 748-751页

作者：梁长林刁云程 Institute of Biophysics Academia Sinica Being 100080 PRC

glutamate (L-glutamic acid, Glu) is widely distributed in the central nervous system (CNS) of the vertebrate. The concentration of glutamate in the CNS is higher than any other commonly recognized neurotransmitter. A ... 详细信息

关键词： glutamate immunocytochemistry visual cortex.

glutamatergic Neurons in the Caudal Zona Incerta Regulate Parkinsonian Motor Symptoms in Mice

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Neuroscience Bulletin 2022年第1期38卷 1-15页

作者： Li-Xuan Li Yu-Lan Li Jin-Tao Wu Ji-Zhou Song Xiao-Ming Li Department of Neurobiology and Department of Neurology of the Second Affiliated Hospital Zhejiang University School of MedicineHangzhou310003China NHC and CAMS Key Laboratory of Medical Neurobiology Ministry of Education Frontier Science Center for Brain Research and Brain-Machine IntegrationSchool of Brain Science and Brain MedicineZhejiang University School of MedicineHangzhou310030China Department of Engineering Mechanics Soft Matter Research Centerand Key Laboratory of Soft Machines and Smart Devices of Zhejiang ProvinceZhejiang UniversityHangzhou310063China

Parkinson’s disease(PD)is the second most common and fastest-growing neurodegenerative disorder.In recent years,it has been recognized that neurotransmitters other than dopamine and neuronal systems outside the basal ganglia are also related to PD pathogenesis.However,little is known about whether and how the caudal zona incerta(ZIc)regulates parkinsonian motor symptoms.Here,we showed that specific glutamatergic but not GABAergic ZIc^(VgluT2) neurons regulated these symptoms.ZIc^(VgluT2) neuronal activation induced time-locked parkinsonian motor symptoms.In mouse models of PD,the ZIc^(VgluT2) neurons were hyperactive and inhibition of their activity ameliorated the motor deficits.ZIc^(VgluT2) neurons monosynaptically projected to the substantia nigra pars reticulata.Incerta-nigral circuit activation induced parkinsonian motor symptoms.Together,our findings provide a direct link between the ZIc,its glutamatergic neurons,and parkinsonian motor symptoms for the first time,help to better understand the mechanisms of PD,and supply a new important potential therapeutic target for PD.

关键词： Parkinson's disease Caudal zona incerta glutamate Substantia nigra pars reticulata Parkinsonian motor symptoms

Glutamine and glutamate: Nonessential or essential amino acids?

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Animal Nutrition 2015年第3期1卷 119-122页

作者： Malcolm Watford Department of Nutritional Sciences Rutgers The State University

Glutamine and glutamate are not considered essential amino acids but they play important roles in maintaining growth and health in both neonates and adults. Although glutamine and glutamate are highly abundant in most feedstuffs there is increasing evidence that they may be limiting during pregnancy, lactation and neonatal growth, particularly when relatively low protein diets are fed. Supplementation of diets with glutamine, glutamate or both at 0.5 to 1.0% to both suckling and recently weaned piglets improves intestinal and immune function and results in better growth. In addition such supplementation to the sow prevents some of the loss of lean body mass during lactation, and increases milk glutamine content. However, a number of important questions related to physiological condition,species under study and the form and amount of the supplements need to be addressed before the full benefits of glutamine and glutamate supplementation in domestic animal production can be realized.

关键词： Amino acid glutamate Glutamine Lactation Pregnancy Growth

Inhibitory effects of HS014 on glutamate release in astrocytes chronically treated with morphine

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Neural Regeneration Research 2010年第19期5卷 1491-1494页

作者： Haichen Chu Zejun Niu Zhao Yang Xuefeng Zhang Department of Anesthesiology Affiliated Hospital of Medical College Qingdao University Qingdao 266003 Shandong Province China Qingdao Institute for Drug Control Qingdao 266000 Shandong Province China Stem Cell Center Affiliated Hospital of Medical College Qingdao University Qingdao 266003 Shandong Province China

Previous studies have confirmed that the number of glial fibrillary acidic protein-positive cells significantly increases during morphine tolerance. However, morphine tolerance is reversed with melanocortin receptor antagonists, and analgesic action is enhanced accordingly. However, these mechanisms remain unclear. In the present study, following addition of morphine to Wistar rat spinal cord astrocytes, glutamate levels in the supematant significantly increased （P 〈 0.05）. At 30-120 minutes following addition of intervention agent to spinal cord astrocytes, naloxone significantly increased glutamate release in morphine-tolerant model cells （P 〈 0.05）, while melanocortin receptor antagonist HS014 decreased glutamate release （P 〈 0.05）. Additional naloxone and HS014 to astrocytes significantly decreased glutamate release compared with additional naloxone alone （P 〈 0.01）. Results from the present study demonstrated that glutamate release was increased in spinal cord astrocytes co-cultured with morphine. Naloxone increased glutamate release, and HS014 reduced glutamate release.

关键词： HS014 naloxone astrocytes morphine glutamate high performance liquid chromatography-tandem quadrupole mass spectrometry

Effect of propofol on glutamate-induced activation and related inflammatory cytokines of astrocytes from spinal cord dorsal horn

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Neural Regeneration Research 2008年第9期3卷 954-957页

作者： Chengming Qin Qing Li Juying Liu Tao Zhu Yong Xiang Department of Anesthesiology Taihe Hospital of Yunyang Medical College Shiyan 442000 Hubei Province China

BACKGROUND： Astrocytes participate in central nervous system-mediated physiological or pathological processes, such as pain. Activated dorsal horn astrocytes from the spinal cord produce nerve active substances and proinflammatory cytokines, such as interleukin-lbeta （IL-1 β ）, IL-6, and tumor necrosis factor- α （TNF-α ）, which play important roles in pain transduction and regulation. OBJECTIVE： To investigate the effects of different doses of propofol on activation of cultured spinal cord dorsal horn astrocytes induced by glutamate, as well as changes in IL-1β, IL-6, and TNF- α, and 1L-10 （anti-inflammatory cytokine） expression in rats, and to explore the dose relationship of propofol. DESIGN, TIME AND SETTING： The cellular and molecular biology experiment was performed at the Central Laboratory of Yunyang Medical College between March 2006 and December 2007. MATERIALS： Forty healthy, Wistar rats, aged 2-3 days, were selected. Propofol was provided by Zeneca, UK; glutamate by Sigma, USA; EPICS XL flow cytometry by Beckman culture, USA; rabbit-anti-mouse glial fibrillary acidic protein （GFAP） antibody kit and inflammatory cytokine detection kit were provided by Zhongshan Biotechnology Company Ltd., Beijing; multimedia color pathologic image analysis system was a product of Nikon, Japan. METHODS： Astrocytes were harvested from T11- L6 spinal cord dorsal horn of Wistar rats and incubated for 3 weeks. The cells were divided into seven groups, according to various treatment conditions： control group was cells cultured in Hank＇s buffered saline solution; intralipid group was cells cultured in intralipid （0.2 mL/L）; glutamate group was cells cultured with 100 u mol/L glutamate; propofol group was cells cultured with 250 u mol/L propofol; three glutamate plus propofol groups were cultured in 100 11 mol/L of glutamate, followed by 5, 25, and 250 u mol/L of propofol 10 minutes later. MAIN OUTCOME MEASURES： GFAP-labeled astrocytes were analyzed using a multimedia pathology imaging analysis system to detect area density （AD

关键词： astrocyte glutamate inflammatory cytokine propofol spinal cord dorsal horn

Effects of glutamate and nimodipine on survival rate of embryonic rat neuronal stem cells cultured in vitro

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Neural Regeneration Research 2008年第12期3卷 1286-1289页

作者： Xiaohong Lu Hailong Fu Qiang Sun Li Cui Dihui Ma Weihong Lin Department of Neurology First Hospital Jinlin University Changchun 1300021 Jilin Province China

BACKGROUND： At least three types of calcium ion channel （T, N, and L） have been recognized in nerve ceils, but only the L type of channel is sensitive to drugs. Theoretically, nimodipine can lead to L-type channel inactivation and prevent calcium ion inflow, thereby exhibiting protective effects on nerve cells. OBJECTIVE： To observe the protective effects of nimodipine on glutamate-induced injury to embryonic rat neural stem cells, and to make a comparison with MK-801, a nonselective glutamate receptor antagonist. DESIGN, TIME AND SETTING： The present in vitro experiment pertaining to neural stem cells was performed at the Department of Neurology, First Hospital, Jilin University between January 2005 and December 2006. MATERIALS： glutamate was sourced from the Shanghai Biological Research Institute of the Chinese Academy of Sciences. Nimodipine was provided by Bayer Company, Germany. Brain tissue was taken from Wistar rats on day 15 of gestation for isolation and culture of neural stem cells. METHODS： Passage 2 neural stem cell spheres were taken for preparation of single cell suspension. The prepared single cell suspension was divided into 4 groups：（1） Normal control, normally cultured. （2） glutamate, cultured with 50, 100, 200, 500, and 1 000 μmol/L glutamate. （3） Nimodipine, received a 30- minute nimodipine [1×（10^-8-10^-2） g/L] culture followed by a glutamate （200 μmol/L） treatment step. （4） MK-801, given as 30- minute MK-801 （100 μmol/L） culture, followed by a glutamate （200 μmol/L） treatment step. MAIN OUTCOME MEASURES： Determination of glutamate-induced cell death by methyl thiazolyl tetrazolium （MTT） assay; calculation of neural stem cell survival rate following addition of nimodipine. RESULTS： The survival rate of neural stem cells was approximately 25.26% following 24 hour 50 μmol/L glutamate culture and gradually decreased as the glutamate dose increased （P 〈 0.05 0.01）. Only 9.27% of neural stem cells survived when the glutamate dose was 1000 μmol/L. The survival rate of neural stern cells was signif

关键词： neural stem cells culture glutamate injury nimodipine protective effects

Nerve growth factor pretreatment against glutamate-induced hippocampal neuronal injury Action mechanism of phosphatase and tensin homologue deleted on chromosome 10

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Neural Regeneration Research 2010年第1期5卷 5-9页

作者： Yae Hu Jiahui Mao Yan Zhu Ailing Zhou Department of Pathophysiology Medical School of Nantong University Nantong 226001 Jiangsu Province China

BACKGROUND： Nerve growth factor （NGF） attenuates glutamate-induced injury to hippocampal neurons, and the human tumor suppressor gene phosphatase and tensin homologue deleted on chromosome 10 （PTEN） promotes neuronal apoptosis. However, effects of PTEN in NGF-mediated neuroprotection against glutamate excitotoxicity remain poorly understood. OBJECTIVE： To investigate the relationship between NGF inhibition of glutamate-induced injury and PTEN. DESIGN, TIME AND SE＇I＇rlNG： The randomized, controlled, in vitro study was performed at the Department of Pathophysiology, Medical School of Nantong University, China from October 2007 to March 2008. MATERIALS： glutamate, NGF, 4, 6-diamidino-2-phenyl-indolediacetate, 3-[4, 5-dimethylthiazol-2-yl]- 2, 5-diphenyl tetrazoliumbromide （M-I-F）, and lactate dehydrogenase kit （Sigma, USA）, fluorescence microscope and inverted phase contrast microscope （Olympus, Japan） were used in this study. METHODS： Hippocampal neurons were obtained from newborn （〈 24 hours） Sprague Dawley rats and cultured for 7 days. The control group was not treated with any intervention factor, the glutamate group was treated with glutamate （0.2 mmol/L）, and NGF groups were treated with NGF （10, 50, 100, and 200 μg/L, respectively） prior to glutamate treatment. MAIN OUTCOME MEASURES： The MTT and lactate dehydrogenase assays were applied to evaluate viability of hippocampal neurons. Morphological changes in hippocampal neurons were observed using an inverted phase-contrast microscope, and neuronal apoptosis was detected by 4, 6-diamidino-2- phenyl-indolediacetate staining. PTEN mRNA and protein expression were measured by reverse transcription-polymerase chain reaction and Western blot analysis, respectively. RESULTS： glutamate （0.2 mmol/L） induced significantly decreased neuronal viability and greater lactate dehydrogenase efflux compared with the control group （P 〈 0.01）. However, compared with the glutamate group, cell viability significantly increased and lactate dehydrogenase efflux decreased in the NGF g

关键词： nerve growth factor glutamate phosphatase and tensin homologue deleted on chromosome 10 hippocampus neurons nerve factor

Genomic structure of metabotropic glutamate receptor 7 and comparison of genomic structures of extracellular domains of mGluR family

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Chinese Science Bulletin 2002年第16期47卷 1330-1336页

作者： Qingfa Wu Wei Dong Xiaohua Qi Weidong Bao Yuxin Niu Yiling Zhang Haiqing Zhang Chong Chen Bin Liu Songnian Hu et al. Chinese Acad Sci Inst Genet Beijing Gen Inst Ctr Human Genome Beijing 100101 Peoples R China

Metabotropic glutamate receptor 7, coupled with a chemical neurotransmitter L-glutamate, plays an important role in the development of many psychiatric and neurological disorders. To study the biological and genetic mechanism of the mGluR7-related diseases, a physical map covering the full-length mGluR7 genomic sequence has been constructed through seed clone screening and fingerprinting database searching. These BAC clones in the physical map have been sequenced with shotgun strategy and assembled by Phred-Phrap-Consed software; the error rate of the final genoniic sequence is less than 0.01%. mGluR7 spans 880 kb genoniic region, the GC content and repeat content of mGluR7 genoniic sequence are 38% and 37.5% respectively. mGluR7 has a typical 'house-keeping' promoter and consists of 11 exons, with introns ranging from 6 kb to 285 kb. mGluR7a and mGluR7b are two known alternatively splicing variants. Comparing the genomic structures of extracellular domains of mGluR family, their genomic structures can

关键词： metabotropic glutamate receptor physical map genome exon intron extracellular domain.

glutamate enhances the expression of vascular endothelial growth factor in cultured SD rat astrocytes

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Journal of Pharmaceutical Analysis 2009年第3期21卷 198-201页

作者： Chong-xiao Liu1,2,Yong Liu1,Wei Shi2,Xin-lin Chen1,Xin-li Xiao1,Ling-yu Zhao1,Yu-mei Tian1,Jun-feng Zhang11. Institute of Neurobiology,Medical School of Xi’an Jiaotong University,Xi’an 710061 2. Department of Neurosurgery,the Second Affiliated Hospital,Medical School of Xi’an Jiaotong University,Xi’an 710004,China. Institute of Neurobiology Medical School of Xi'an Jiaotong University Xi'an 710061 China Department of Neurosurgery Second Affiliated Hospital Medical School of Xi'an Jiaotong University Xi'an 710004 China

Objective To study the effect of glutamate on the expression of vascular endothelial growth factor (VEGF) mRNA and protein in cultured rat astrocytes. Methods Cultured rat astrocytes were randomly divided into 6 groups:control group (C),glutamate group (G),QA group (Q),DCG-IV group (D),L-AP4 group (L) and glutamate+MCPG group (G+M). Cells were cultured under nomoxic condition (95% air,5% CO2). RT-PCR and ELISA methods were used to detect the expression of VEGF mRNA and protein in cultured astrocytes,respectively. G+M group was preincubated with 1mM MCPG for 30 min prior to the stimulation with glutamate. There were 7 time points at 0,4,8,12,16,24 and 48 h in each group except G+M group. Results The expression of VEGF mRNA and protein did not differ significantly among D group,L group and C group. Different from that in C group,the expression of VEGF mRNA and protein could be enhanced both in a dose-dependent and time-dependent manner in G group and Q group. Meanwhile,the enhanced expression of VEGF mRNA and protein in G group was completely suppressed by MCPG after 24 h. Conclusion glutamate can increase the expression of VEGF mRNA and protein in cultured astrocytes,which may be due to the activation of group I metabotropic glutamate receptors in astrocytes.

关键词： glutamate metabotropic glutamate receptor vascular endothelial growth factor (VEGF) astrocyte

Bis(7)-Tacrine, a Promising Anti-Alzheimer's Agent,Attenuates glutamate-Induced Cell Injury in Primary Cultured Cerebrocortical Neurons of Rats

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Wuhan University Journal of Natural Sciences 2001年第3期6卷 737-741页

作者： Zhang Bai fang,Peng Fang fang,Zhang Jiang zhou,Wu Dong cheng  Biochemistry Department, School of Medicine, Wuhan University, Wuhan 430071, China Biochemistry Department School of Medicine Wuhan University Wuhan China

The effects of bis(7) tacrine, a novel dimeric acetylcholinesterase (AChE) inhibitor, on glutamate induced cell injury were investigated in primary cerebral cortical neurons of rats. Exposure of cultured neurons (12 days after plating) to 0.5 mmol/L glutamate for 30 min resulted in significant cell damage. Pretreatment with bis(7) tacrine (0.03 1.0 μmol/L) reduced the glutamate induced neurotoxicity in a concentration dependent manner and the maximal response was seen at 1 μmol/L with approximately 30% protection. A receptor binding assay showed that bis(7) tacrine can completely displace MK 801 binding to rat cortical membrane with an IC 50 of 0.57 μmol/L. These findings suggest that bis(7) tacrine can directly interact with N methyl D aspartate receptor channel complex, which may contribute to the inhibitor's protective effects against glutamate induced excitotoxicity. Thus, it is possible that anti glutamate/anti AChE synergism is responsible for potentially better Alzheimer's therapy of bis(7) tacrine relative to tacrine.

关键词： bis(7) tacrine tacrine cholinesterase inhibitor glutamate primary neuronal cell culture