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glutamate receptors and glutamatergic signalling in the peripheral nerves

Neural Regeneration Research 2020年第3期15卷 438-447页

作者： Ting-Jiun Chen Maria Kukley Center for Neuroscience Research Children’s Research InstituteChildren’s National Medical CentreWashingtonDCUSA Group of Neuron Glia Interaction University of TübingenTübingenGermany Research Institute of Ophthalmology Tübingen University HospitalTübingenGermany

In the peripheral nervous system,the vast majority of axons are accommodated within the fibre bundles that constitute the peripheral nerves.Axons within the nerves are in close contact with myelinating glia,the Schwann cells that are ideally placed to respond to,and possibly shape,axonal activity.The mechanisms of intercellular communication in the peripheral nerves may involve direct contact between the cells,as well as signalling via diffusible substances.Neurotransmitter glutamate has been proposed as a candidate extracellular molecule mediating the cross-talk between cells in the peripheral nerves.Two types of experimental findings support this idea:first,glutamate has been detected in the nerves and can be released upon electrical or chemical stimulation of the nerves;second,axons and Schwann cells in the peripheral nerves express glutamate receptors.Yet,the studies providing direct experimental evidence that intercellular glutamatergic signalling takes place in the peripheral nerves during physiological or pathological conditions are largely missing.Remarkably,in the central nervous system,axons and myelinating glia are involved in glutamatergic signalling.This signalling occurs via different mechanisms,the most intriguing of which is fast synaptic communication between axons and oligodendrocyte precursor cells.glutamate receptors and/or synaptic axon-glia signalling are involved in regulation of proliferation,migration,and differentiation of oligodendrocyte precursor cells,survival of oligodendrocytes,and re-myelination of axons after damage.Does synaptic signalling exist between axons and Schwann cells in the peripheral nerves?What is the functional role of glutamate receptors in the peripheral nerves?Is activation of glutamate receptors in the nerves beneficial or harmful during diseases?In this review,we summarise the limited information regarding glutamate release and glutamate receptors in the peripheral nerves and speculate about possible mechanisms of glutamatergic signalling in the nerves.We highli

关键词： AMPA receptors axons glutamate metabotropic glutamate receptors myelination nerve injury NMDA receptors peripheral nervous system PNS Schwann cells synaptic signalling

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glutamate receptor delocalization in postsynaptic membrane and reduced hippocampal synaptic plasticity in the early stage of Alzheimer's disease

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Neural Regeneration Research 2019年第6期14卷 1037-1045页

作者： Ning Li Yang Li Li-Juan Li Ke Zhu Yan Zheng Xiao-Min Wang Department of Neurobiology Capital Medical University Key Laboratory for Neurodegenerative Disorders of the Ministry of Education Capital Medical University Beijing Institute for Brain Disorders Department of Physiology Capital Medical University

Mounting evidence suggests that synaptic plasticity provides the cellular biological basis of learning and memory, and plasticity deficits play a key role in dementia caused by Alzheimer's disease. However, the mechanisms by which synaptic dysfunction contributes to the pathogenesis of Alzheimer's disease remain unclear. In the present study, Alzheimer's disease transgenic mice were used to determine the relationship between decreased hippocampal synaptic plasticity and pathological changes and cognitive-behavioral deterioration, as well as possible mechanisms underlying decreased synaptic plasticity in the early stages of Alzheimer's disease-like diseases. APP/PS1 double transgenic(5 XFAD; Jackson Laboratory) mice and their littermates(wild-type, controls) were used in this study. Additional 6-weekold and 10-week-old 5 XFAD mice and wild-type mice were used for electrophysiological recording of hippocampal dentate gyrus. For10-week-old 5 XFAD mice and wild-type mice, the left hippocampus was used for electrophysiological recording, and the right hippocampus was used for biochemical experiments or immunohistochemical staining to observe synaptophysin levels and amyloid beta deposition levels. The results revealed that, compared with wild-type mice, 6-week-old 5 XFAD mice exhibited unaltered long-term potentiation in the hippocampal dentate gyrus. Another set of 5 XFAD mice began to show attenuation at the age of 10 weeks, and a large quantity of amyloid beta protein was accumulated in hippocampal cells. The location of α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor and N-methyl-D-aspartic acid receptor subunits in synaptosomes was decreased. These findings indicate that the delocalization of postsynaptic glutamate receptors and an associated decline in synaptic plasticity may be key mechanisms in the early onset of Alzheimer's disease. The use and care of animals were in strict accordance with the ethical standards of the Animal Ethics Committee of Capital Medical University,China on December 17, 2

关键词： nerve regeneration Alzheimer’s disease synaptic plasticity hippocampus learning and memory long-term potentiation βamyloid glutamate receptor synaptic strength neural regeneration

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glutamate and aspartate alleviate testicular/epididymal oxidative stress by supporting antioxidant enzymes and immune defense systems in boars

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Science China(Life Sciences) 2020年第1期63卷 116-124页

作者： Wenjie Tang Jian Wu Shunshun Jin Liuqin He Qinlu Lin Feijun Luo Xingguo He Yanzhong Feng Binsheng He Pingping Bing Tiejun Li Yulong Yin Hunan International Joint Laboratory of Animal Intestinal Ecology and Health Laboratory of Animal Nutrition and Human HealthCollege of Life SciencesHunan Normal UniversityChangsha 410081China Key Laboratory of Agro-ecological Processes in Subtropical Region Institute of Subtropical AgricultureChinese Academy of SciencesHunan Provincial Key Laboratory of Animal Nutritional Physiology and Metabolic ProcessNational Engineering Laboratory for Pollution Control and Waste Utilization in Livestock and Poultry ProductionChangsha 410125China National Engineering Laboratory for Deep Process of Rice and Byproducts Hunan Key Laboratory of Grain-oil Deep Process and Quality ControlHunan Key Laboratory of Processed Food for Special Medical PurposeCollege of Food Science and EngineeringCentral South University of Forestry and TechnologyChangsha 410004China Academics Working Station at The First Affiliated Hospital Changsha Medical UniversityChangsha 410219China Sichuan Academy of Animal Sciences Animal Breeding and Genetics Key Laboratory of Sichuan ProvinceChengdu 610066China ^Changsha Green LecrfBiotechnology Co. Ltd.Changsha 610066Hunan Heilongjiang Academy of Agricultural Sciences Harbin 150086China

Several potential oxidative agents have damaging effects on mammalian reproductive systems.This study was conducted to investigate the effects of glutamate(Glu)and aspartate(Asp)supplementation on antioxidant enzymes and immune defense systems in the outer scrotum of boars injected with H2O2.A total of 24 healthy boars were randomly divided into 4 treatment groups:control(basal diet,saline-treated),H2O2(basal diet,H2O2-challenged outer scrotum(1 m L kg^–1 BW)),Glu(basal diet+2%Glu,H2O2-challenged),and Asp(basal diet+2%Asp,H2O2-challenged).Our results showed that both Glu and Asp supplementation improved testicular morphology and decreased the genital index in the H2O2-treated boars.Glu and Asp administration increased the antioxidant enzyme activities and affected the testicular inflammatory cytokine secretion but had no effect on sex hormone levels.Furthermore,the m RNA expression of CAT,Cu Zn SOD,and GPx4 was altered in the testes and epididymis of boars treated with Asp and Glu.Glu and Asp supplementation also modulated the expression of TGF-β1,IL-10,TNF-α,IL-6 and IL-1βin the testis and epididymis.These results indicate that dietary Glu and Asp supplementation might enhance antioxidant capacity and regulate the secretion and expression of inflammatory cytokines to protect the testes and epididymis of boars against oxidative stress.

关键词： glutamate aspartate boars oxidative stress inflammatory cytokines

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Adipose mesenchymal stem cell-derived extracellular vesicles reduce glutamate-induced excitotoxicity in the retina

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Neural Regeneration Research 2023年第10期18卷 2315-2320页

作者： Tian-Qi Duan Zhao-Lin Gao Ai-Xiang Luo Dan Chen Jian-Bin Tong Ju-Fang Huang Department of Anatomy and Neurobiology School of Basic Medical SciencesCentral South UniversityChangshaHunan ProvinceChina Hunan Province Key Laboratory of Brain Homeostasis Third Xiangya HospitalCentral South UniversityChangshaHunan ProvinceChina

Adipose mesenchymal stem cells(ADSCs)have protective effects against glutamate-induced excitotoxicity,but ADSCs are limited in use for treatment of optic nerve injury.Studies have shown that the extracellular vesicles(EVs)secreted by ADSCs(ADSC-EVs)not only have the function of ADSCs,but also have unique advantages including non-immunogenicity,low probability of abnormal growth,and easy access to target cells.In the present study,we showed that intravitreal injection of ADSC-EVs substantially reduced glutamate-induced damage to retinal morphology and electroretinography.In addition,R28 cell pretreatment with ADSC-EVs before injury inhibited glutamate-induced overload of intracellular calcium,downregulation ofα-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid receptor(AMPAR)subunit GluA2,and phosphorylation of GluA2 and protein kinase C alpha in vitro.A protein kinase C alpha agonist,12-O-tetradecanoylphorbol 13-acetate,inhibited the neuroprotective effects of ADSC-EVs on glutamate-induced R28 cells.These findings suggest that ADSCEVs ameliorate glutamate-induced excitotoxicity in the retina through inhibiting protein kinase C alpha activation.

关键词： adipose mesenchymal stem cells calcium overload electroretinography excitotoxicity extracellular vesicles GluA2 glutamate protein kinase C alpha R28 cells retina retinal ganglion cell

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glutamate in cancers:from metabolism to signaling

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The Journal of Biomedical Research 2020年第4期34卷 260-270页

作者： Haowei Yi Geoff Talmon Jing Wang Department of Genetics Cell Biology and AnatomyUniversity of Nebraska Medical CenterOmahaNE 68198USA. Department of Pathology and Microbiology University of Nebraska Medical CenterOmahaNE 68198USA. Eppley Institute for Research in Cancer and Allied Diseases University of Nebraska Medical CenterOmahaNE 68198USA.

Glutamine and glutamate are major bioenergy substrates for normal and cancer cell growth.Cancer cells need more biofuel than normal tissues for energy supply,anti-oxidation activity and biomass production.Genes related to metabolic chains in many cancers are somehow mutated,which makes cancer cells more glutamate dependent.Meanwhile,glutamate is an excitatory neurotransmitter for conducting signals through binding with different types of receptors in central neuron system.Interestingly,increasing evidences have shown involvement of glutamate signaling,guided through their receptors,in human malignancy.Dysregulation of glutamate transporters,such as excitatory amino acid transporter and cystine/glutamate antiporter system,also generates excessive extracellular glutamate,which in turn,activates glutamate receptors on cancer cells and results in malignant growth.These features make glutamate an attractive target for anti-cancer drug development with some glutamate targeted but blood brain barrier impermeable anti-psychosis drugs under consideration.We discussed the relevant progressions and drawbacks in this field herein.

关键词： glutamate cancers metabolism glutamate receptors glutamate transporters

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Polygalasaponin F protects hippocampal neurons against glutamate-induced cytotoxicity

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Neural Regeneration Research 2022年第1期17卷 178-184页

作者： Chong Sun Xin-Cheng Cao Zhi-Yang Liu Chao-Lin Ma Bao-Ming Li Laboratory of Cognitive Function and Disorder Institute of Life ScienceNanchang UniversityNanchangJiangxi ProvinceChina Institute of Brain Science and Department of Psychology School of EducationHangzhou Normal UniversityHangzhouZhejiang ProvinceChina

Excess extracellular glutamate leads to excitotoxicity,which induces neuronal death through the overactivation of N-methyl-D-aspartate receptors(NMDARs).Excitotoxicity is thought to be closely related to various acute and chronic neurological disorders,such as stroke and Alzheimer’s disease.Polygalasaponin F(PGSF)is a triterpenoid saponin monomer that can be isolated from Polygala japonica,and has been reported to protect cells against apoptosis.To investigate the mechanisms underlying the neuroprotective effects of PGSF against glutamateinduced cytotoxicity,PGSF-pretreated hippocampal neurons were exposed to glutamate for 24 hours.The results demonstrated that PGSF inhibited glutamate-induced hippocampal neuron death in a concentration-dependent manner and reduced glutamate-induced Ca^(2+)overload in the cultured neurons.In addition,PGSF partially blocked the excess activity of NMDARs,inhibited both the downregulation of NMDAR subunit NR2A expression and the upregulation of NMDAR subunit NR2B expression,and upregulated the expression of phosphorylated cyclic adenosine monophosphate-responsive element-binding protein and brain-derived neurotrophic factor.These findings suggest that PGSF protects cultured hippocampal neurons against glutamate-induced cytotoxicity by regulating NMDARs.The study was approved by the Institutional Animal Care Committee of Nanchang University(approval No.2017-0006)on December 29,2017.

关键词： BDNF Ca^(2+)homeostasis excitotoxicity glutamate hippocampal neurons pCREB polygalasaponin F neuroprotection NR2A NR2B

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Glutamine,glutamate,and aspartate differently modulate energy homeostasis of small intestine under normal or low energy status in piglets

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Animal Nutrition 2022年第1期8卷 216-226页

作者： Jing Wang Nan Wang Ming Qi Jianjun Li Bie Tan College of Animal Science and Technology Hunan Agricultural UniversityChangsha 410128HunanChina Animal Nutrition and Human Health Laboratory Hunan Provincial Key Laboratory of Animal Intestinal Function and RegulationSchool of Life SciencesHunan Normal UniversityChangsha 410081HunanChina Laboratory of Animal Nutritional Physiology and Metabolic Process Key Laboratory of Agroecological Processes in Subtropical RegionNational Engineering Laboratory for Pollution Control and Waste Utilization in Livestock and Poultry ProductionInstitute of Subtropical AgricultureChinese Academy of SciencesChangsha 410125HunanChina University of Chinese Academy of Sciences Beijing 10008China

Weaning stress may cause reduced energy intake for maintenance of mucosal structure.Gln,Glu,and Asp are major energy sources for the small intestine.This study investigated whether Gln,Glu,and Asp improve the intestinal morphology via regulating the energy metabolism in weaning piglets.A total of 198 weaned piglets were assigned to 3 treatments:Control(Basal diet+1.59%L-Ala);T1(Basal diet+1%L-Gln+0.5%L-Glu+0.1%L-Asp);T2(Low energy diet+1%L-Gln+0.5%L-Glu+0.1%L-Asp).Jejunum and ileum were obtained on d 5 or 21 post-weaning.T1 enhanced growth performance.T1 and T2 treatments improved small intestinal morphology by increasing villus height,goblet cell number and decreasing crypt depth.Days post-weaning affected the efficacy of T2,but not T1,on energy metabolism.At normal energy supplementation,Gln,Glu,and Asp restored small intestinal energy homeostasis via replenishing the Krebs'cycle and down-regulating the AMPK(adenosine monophosphate activated protein kinase)pathway.As these are not sufficient to maintain the intestinal energy-balance of piglets fed with a low energy diet on d 5 post-weaning,the AMPK,glycolysis,beta-oxidation,and mitochondrial biogenesis are activated to meet the high energy demand of enterocytes.These data indicated that Gln,Glu,and Asp could restore the energy homeostasis of intestinal mucosa of weaning piglets under normal energy fed.Low energy feeding may increase the susceptibility of piglets to stress,which may decrease the efficacy of Gln,Glu,and Asp on the restoration of energy balance.These findings provide new information on nutritional intervention for insufficient energy intake in weaning piglets.

关键词： Glutamine glutamate Aspartate Small intestine Energy metabolism

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glutamate transporters, EAAT1 and EAAT2, are potentially important in the pathophysiology and treatment of schizophrenia and affective disorders

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World Journal of Psychiatry 2018年第2期8卷 51-63页

作者： Georgia M Parkin Madhara Udawela Andrew Gibbons Brian Dean Molecular Psychiatry Laboratory the Florey Institute of Neuroscience and Mental Health CRC for Mental Health Research Centre for Mental Health the Faculty of Health Arts and Design Swinburne University

glutamate is the predominant excitatory neurotransmitter in the human brain and it has been shown that prolonged activation of the glutamatergic system leads to nerve damage and cell death. Following release from the pre-synaptic neuron and synaptic transmission, glutamate is either taken up into the presynaptic neuron or neighbouring glia by transmembrane glutamate transporters. Excitatory amino acid transporter(EAAT) 1 and EAAT2 are Na+-dependant glutamate transporters expressed predominantly in glia cells of the central nervous system. As the most abundant glutamate transporters, their primary role is to modulate levels of glutamatergic excitability and prevent spill over of glutamate beyond the synapse. This role is facilitated through the binding and transportation of glutamate into astrocytes and microglia. The function of EAAT1 and EAAT2 is heavily regulated at the levels of gene expression, post-transcriptional splicing, glycosylation states and cell-surface trafficking of the protein. Both glutamatergic dysfunction and glial dysfunction have been proposed to be involved in psychiatric disorder. This review will present an overview of the roles that EAAT1 and EAAT2 play in modulating glutamatergic activity in the human brain, and mount an argument that these two transporters could be involved in the aetiologies of schizophrenia and affective disorders as well as represent potential drug targets for novel therapies for those disorders.

关键词： Glia Excitatory amino acid transporter Psychiatry Affective disorders glutamate transporter glutamate Schizophrenia

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glutamate Transporter 1-mediated Antidepressant-like Effect in a Rat Model of Chronic Unpredictable Stress

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2014年第6期34卷 838-844页

作者：陈建新姚丽华徐碧波钱坤王惠玲刘忠纯王晓萍王高华 Department of Psychiatry Renmin Hospital Wuhan University Department of Psychology Faculty of Education Hubei University Department of Obstetrics and Gynecology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology

In recent years, more attention has been paid to the role of the glutamate transporter 1 （GLT-1, EAAT2） in major depressive disorder （MDD）. However, experimental data on brain GLT-1 levels are, to some extent, inconsistent in human postmortem and animal studies, These discrepancies imply that the role of GLT-1 in the pathophysiology of MDD and the action of antidepressants remain obscure. This work was designed to study the impact of chronic unpredictable stress （CUS） for 2 ses- sions per day for 35 days and four weeks of fluoxetine （FLX） on depressive-like behaviors in rats, as well as the concomitant expression of the GLT-1 protein in the hippocampus. Behavioral changes were assessed by the sucrose preference and open field tests. GLT-1 levels were detected by immunohisto- chemistry and Western blot analysis. Our study demonstrated that the animals exposed to CUS showed depressive-like behaviors and exhibited a significant decrease in GLT-1 expression in the hippocampus. Chronic FLX treatment reversed the behavioral deficits and the CUS-induced decrease in GLT-1 levels. Taken together, our results support the reduction of GLT-1 in human postmortem studies in MDD and suggest that GLT-1 may be involved in the antidepressant activity of FLX. Our studies further support the notion that GLT-1 is an attractive candidate molecule associated with the fundamental processes of MDD and may be a potential, and novel pharmacological target for the treatment of MDD.

关键词： chronic unpredictable stress glutamate transporter 1 glutamate fluoxetine hippocampus

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Achyranthes bidentata polypeptides prevent apoptosis by inhibiting the glutamate current in cultured hippocampal neurons

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Neural Regeneration Research 2020年第6期15卷 1086-1093页

作者： Rong-Lu Pan Wen-Qing Hu Jie Pan Li Huang Cheng-Cheng Luan Hong-Mei Shen Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education and Institute of Nautical Medicine Co-Innovation Center of NeuroregenerationNantong UniversityNantongJiangsu ProvinceChina Department of Neurobiology Physiology and BehaviorCollege of Biological ScienceDavisCAUSA Affiliated Mental Health Center of Nantong University Nantong Brain HospitalNantongJiangsu ProvinceChina

glutamate-induced excitotoxicity plays a critical role in the neurological impairment caused by middle cerebral artery occlusion.Achyranthes bidentata polypeptides have been shown to protect against neurological functional damage caused by middle cerebral artery occlusion,but the underlying neuroprotective mechanisms and the relationship to glutamate-induced excitotoxicity remain unclear.Therefore,in the current study,we investigated the protective effects of Achyranthes bidentata polypeptides against glutamate-induced excitotoxicity in cultured hippocampal neurons.Hippocampal neurons were treated with Mg^2+-free extracellular solution containing glutamate(300μM)for 3 hours as a model of glutamate-mediated excitotoxicity(glutamate group).In the normal group,hippocampal neurons were incubated in Mg^2+-free extracellular solution.In the Achyranthes bidentata polypeptide group,hippocampal neurons were incubated in Mg^2+-free extracellular solution containing glutamate(300μM)and Achyranthes bidentata polypeptide at different concentrations.At 24 hours after exposure to the agents,3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and Hoechst 33258 staining were used to assess neuronal viability and nuclear m'orphology,respectively.Caspase-3 expression and activity were evaluated using western blot assay and colorimetric enzymatic assay,respectively.At various time points after glutamate treatment,reactive oxygen species in cells were detected by H2 DCF-DA,and mitochondrial membrane potential was detected by rhodamine 123 staining.To examine the effect of Achyranthes bidentata polypeptides on glutamate receptors,electrophysiological recording was used to measure the glutamate-induced inward current in cultured hippocampal neurons.Achyranthes bidentata polypeptide decreased the percentage of apoptotic cells and reduced the changes in caspase-3 expression and activity induced by glutamate.In addition,Achyranthes bidentata polypeptide attenuated the amplitude of the glutamate-induced current.Furthermore,t

关键词： Achyranthes bidentata polypeptides apoptosis caspase-3 excitotoxicity glutamate receptors mitochondrial dysfunction mitochondrial membrane potential neuroprotection reactive oxygen species staurosporine

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