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Catgut implantation at acupoints increases the expression of glutamate aspartate transporter and glial glutamate transporter-1 in the brain of rats with spasticity after stroke

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Neural Regeneration Research 2018年第6期13卷 1013-1018页

作者： Rui-Qing Li Ming-Yue Wan Jing Shi Hui-Ling Wang Fei-Lai Liu Cheng-Mei Liu Jin Huang Ren-Chao Liu Le Ma Xiao-Dong Feng Rehabilitation Center First Affiliated Hospital of Henan University of Traditional Chinese Medicine Major in Rehabilitation Medicine and Physiotherapy Henan University of Traditional Chinese Medicine Department of Oncology Third People's Hospital of Luoyang

Catgut implantation at acupoints has been shown to alleviate spasticity after stroke in rats.However,the underlying mechanisms are poorly understood.In this study,we used the rat middle cerebral artery occlusion model of stroke.Three days after surgery,absorbable surgical catgut sutures were implanted at Dazhui（GV14）,Jizhong（GV6）,Houhui,Guanyuan（CV4）and Zhongwan（CV12）.The Zea Longa score was used to assess neurological function.The Modified Ashworth Scale was used to evaluate muscle tension.The 2,3,5-triphenyl-tetrazolium chloride assay was used to measure infarct volume.Immunohistochemical staining was performed for glutamate aspartate transporter（GLAST）and glial glutamate transporter-1（GLT-1）expression.Western blot assay was used to analyze the expression of GLAST and GLT-1.Reverse transcription and polymerase chain reaction were carried out to assess the expression of GLAST and GLT-1m RNAs.After catgut implantation at the acupoints,neurological function was substantially improved,muscle tension was decreased,and infarct volume was reduced in rats with spasticity after stroke.Furthermore,the expression of GLAST and GLT-1 m RNAs was increased on the injured（left）side.Our findings demonstrate that catgut implantation at acupoints alleviates spasticity after stroke,likely by increasing the expression of GLAST and GLT-1.

关键词： nerve regeneration stroke Dazhui （GV14） lizhong （GV6） Houhui Guanyuan （CV4） Zhongwan （CV12） catgut implantation at acupoints limb spasm glutamate transporter neural regeneration

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Astrocyte-neuron communication mediated by the Notch signaling pathway:focusing on glutamate transport and synaptic plasticity

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Neural Regeneration Research 2023年第10期18卷 2285-2290页

作者： Ke-Xin Li Meng Lu Meng-Xu Cui Xiao-Ming Wang Yang Zheng Department of Radiology Shengjing Hospital of China Medical UniversityShenyangLiaoning ProvinceChina

Maintaining glutamate homeostasis after hypoxic ischemia is important for synaptic function and neural cell activity,and regulation of glutamate transport between astrocyte and neuron is one of the important modalities for reducing glutamate accumulation.However,further research is needed to investigate the dynamic changes in and molecular mechanisms of glutamate transport and the effects of glutamate transport on synapses.The aim of this study was to investigate the regulatory mechanisms underlying Notch pathway mediation of glutamate transport and synaptic plasticity.In this study,Yorkshire neonatal pigs(male,age 3 days,weight 1.0–1.5 kg,n=48)were randomly divided into control(sham surgery group)and five hypoxic ischemia subgroups,according to different recovery time,which were then further subdivided into subgroups treated with dimethyl sulfoxide or a Notch pathway inhibitor(N-[N-(3,5-difluorophenacetyl-l-alanyl)]-S-phenylglycine t-butyl ester).Once the model was established,immunohistochemistry,immunofluorescence staining,and western blot analyses of Notch pathway-related proteins,synaptophysin,and glutamate transporter were performed.Moreover,synapse microstructure was observed by transmission electron microscopy.At the early stage(6–12 hours after hypoxic ischemia)of hypoxic ischemic injury,expression of glutamate transporter excitatory amino acid transporter-2 and synaptophysin was downregulated,the number of synaptic vesicles was reduced,and synaptic swelling was observed;at 12–24 hours after hypoxic ischemia,the Notch pathway was activated,excitatory amino acid transporter-2 and synaptophysin expression was increased,and the number of synaptic vesicles was slightly increased.Excitatory amino acid transporter-2 and synaptophysin expression decreased after treatment with the Notch pathway inhibitor.This suggests that glutamate transport in astrocytes-neurons after hypoxic ischemic injury is regulated by the Notch pathway and affects vesicle release and synaptic plasticity through the expression of synaptop

关键词： astrocyte astrocyte-neuron communication glutamate glutamate transporter hypoxic-ischemic injury magnetic resonance spectroscopy neonate Notch signaling pathway plasticity synapse

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Dynamic expression of cerebral cortex and hippocampal glutamate transporters in a rat model of chest compression-induced global cerebral ischemia

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Neural Regeneration Research 2012年第2期7卷 125-130页

作者： Qinhua Guo Jin Lan Weiqiao Zhang Pin Guo Liemei Guo Zhiqiang Li Yongming Qiu Department of Neurosurgery Renji Hospital Shanghai Jiao Tong University School of Medicine Shanghai 200127 China Central Hospital of Fengxian District Shanghai Neurological Research Institute of Anhui University of Science ＆ Technology Shanghai201400 China

The present study established a rat model of global cerebral ischemia induced by chest compression for six minutes to dynamically observe expressional changes of three glutamate transporters in the cerebral cortex and hippocampus. After 24 hours of ischemia, expression of glutamate transporter-1 significantly decreased in the cerebral cortex and hippocampus, which was accompanied by neuronal necrosis. At 7 days post-ischemia, expression of excitatory amino acid carrier 1 decreased in the hippocampal CA1 region and cortex, and was accompanied by apoptosis Expression of glutamate-aspartate transporter remained unchanged at 6 hours 7 days after ischemia. These results suggested that glutamate transporter levels were altered at different periods of cerebral ischemia.

关键词： apoptosis excitatory amino acid carrier 1 global cerebral ischemia glutamate-aspartate transporter glutamate transporter glutamate transporter-1 neuroprotection

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A mRNA molecule encoding truncated excitatory amino acid carrier l(EAAC1)protein(EAAC2)is transcribed from an independent promoter but not analternative splicing event

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Cell Research 2002年第Z1期 257-262页

作者： XIAO PING JIN, JI BIN PENG, FANG HUANG, YA NI ZHU, JIAN FEI*, LI HE GUO*Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 320 Yueyang Road, Shanghai

glutamate transporter EAACl removes excitatory neurotransmitter in central nervous system, and also absorbs glutamate in epithelia of intestine, kidney, liver and heart for normal cell growth. When a mouse cDNA was screened using EAACl cDNA fragment as probe in our lab, a transcript (GenBank U75214) encoding an EAACl protein with 148 residues truncated at N-terminal was cloned and named as EAAC2. Sequence analysis shows that EAAC2 has it’s own start code and unique 5’UTR that is different from that of EAACl. A mouse genomic library was screened and a positive clone including EAACl CDS was sequenced (GenBank AF 322393) and indicates that normal EAACl transcript (GenBank U73521) is transcribed from 10 exons in terms of exon Ⅰ, Ⅱ, Ⅲ, Ⅳ, Ⅴ, Ⅵ, Ⅶ, Ⅷ,Ⅸ, Ⅹ, and EAAC2 transcript is consisted by exons from IV to IX as same as that of EAACl and with its unique exon β upstream to exon Ⅳ and exon δ downstream to IX. EAAC2 transcript has a cluster of transcriptional start sites not overlapping with the t

关键词： genomic organization glutamate transporter transcriptional start sites EAACl.

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glutamate transporters and alcohol affect long-tem depression at the cerebellar parallel fiber-Purkinje cell synapse

Glutamate transporters and alcohol affect long-tem depressio...

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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： Li-Da SU~(1 2 3) Cheng-Long SUN~(1 2) Ying-Hong HU~3 Ying SHEN~(1 2 *) 1 Department of Neurobiology / Institute of Neuroscience Zhejiang University School of Medicine Hangzhou Zhejiang 310058 China 2 Key laboratory of Medical Neurobiology of Ministry of Health of China 3 Neuroscience care unit the Second affiliated hospital of Zhejiang University School of Medcine Hangzhou 310009 China

＜正＞Objective Metabotropic glutamate receptor 1（mGluR1） shows highest densities at the edge of the post- synaptic density and is required for distinct forms of synaptic plasticity expressed at parallel fiber and climbing fiber synapses in the cerebellum.Most glutamate transporters（termed as EAAT1-4）,except EAAT5,are distributed in molecular layer of adult cerebellum,especially at the excitatory synapses in Purkinje cells.It is widely proposed that glutamate reuptake facilitates chemical synaptic transmission by limiting receptor activation and by recycling released neurotransmitter molecules.Thus,it is of interest to investigate possible roles of EAAT4 in Purkinje cell LTD.Acute alcohol consumption causes deficits in motor coordination and gait,suggesting that cerebellum plays a role in the fine adjustment of movements.It has previously been shown that ethanol modulates inhibitory transmission in the cerebellum and affects synaptic transmission at excitatory climbing fiber to Purkinje cell synapses.However,it has not been well examined how acutely ethanol application affects Purkinje cell LTD.Methods By using whole-cell patch clamp technique combining pharmacologically applying DL-TBOA,D-aspartate and alcohol,we aimed to focus on contribution of EAAT4 and alcohol on properties of EPSC and LTD in Purkinje cells in cerebellar slices.Results（1） Bath application of 300 liM TBOA slightly decreased peak amplitude of EPSCl by（6.8±0.4%） and markedly prolonged EPSC.（2） LTD induced in the presence of TBOA in external saline and 20 mM aspartate in the internal saline were much enhanced compared to control LTD at the time point of 25 min,suggesting that blockade of EAAT4 significandy enhanced the mGluR-dependant LTD in climbingfiber -Purkinje cell synapses.（3） Inhibition of glutamate transporter by bath application of 300μM TBOA during the tetanus and inhibition of EAAT4 by internal 20 mM Asp could rescue failed climbing fiber-Purkinje cell LTD.（4） Short-term application of 50 mM alcohol during tetanus selectively blocked par

关键词： glutamate transporter EAAT4 alcohol Purkinje cell long-term depression metabotropic glutamate receptor

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The effect of PAMd on EAAC1mRNA expression of hippocampus neurons of cerebral ischemia in rat

The effect of PAMd on EAAC1mRNA expression of hippocampus ne...

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第十五届国际药理学大会

作者： lianjun Guo Tie Sun Xuling Xu Ling Qu

＜正＞ AIM: To study the effect of PAMD on EAAC1 mRNA expression in hippocampus after cerebral ischemi. METHODS: Focal cerebral ischemia model was induced by transient occlusion of the middle cerebral artery. After MCAO 2h, PAMd （10mg·kg-1） was administered. The effect of PAMd on hippocampal neuronal glutamate transporter EAAC1 mRNA expression in ischemic rats by RT - PCR was observed. RESULTS: The rats showed significant neurological deficit in 3h after MCAO. 24h after ischemia, the score was was 2.17 ± 0.42. with PAMd the score was was 1.18 ± 0.30. there were significant difference compared with the ischemia group;In 24h after MCAO. the infarct volume was 25.9 ± 2.9 %. PAMd（ 10mg · kg-1 ） could reduce infarct volume to 22. 1 ± 3. 8%;The EAAClmRNA expression of ischemic hippocampal neurons was increased in 24h after ischemia, and PAMd could reduce EAAClmRNA expression CONCLUSION: The results suggested PAMd could reduce Neurological evaluation、 infarct volume and EAAClmRNA expression of the ichemic rats.

关键词： cerebral ischemia glutamate transporter EAACl mRNA PAMd

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