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Journal articles on the topic 'Glutamate transporter GLAST'

Author: Grafiati

Published: 4 June 2021

Last updated: 21 February 2023

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1

Chen, Zhiqiang, Sharon G. Kujawa, and William F. Sewell. "Functional Roles of High-Affinity Glutamate Transporters in Cochlear Afferent Synaptic Transmission in the Mouse." Journal of Neurophysiology 103, no. 5 (May 2010): 2581–86. http://dx.doi.org/10.1152/jn.00018.2010.

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In the cochlea, afferent transmission between inner hair cells and auditory neurons is mediated by glutamate receptors. Glutamate transporters located near the synapse and in spiral ganglion neurons are thought to maintain low synaptic levels of glutamate. We analyzed three glutamate transporter blockers for their ability to alter the effects of glutamate, exogenously applied to the synapse via perfusion of the scala tympani of the mouse, and compared that action to their ability to alter the effects of intense acoustic stimulation. Threo-beta-benzyloxyaspartate (TBOA) is a broad-spectrum glut

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2

SARTHY, VIJAY P., V. JOSEPH DUDLEY, and KOHICHI TANAKA. "Retinal glucose metabolism in mice lacking the L-glutamate/aspartate transporter." Visual Neuroscience 21, no. 4 (July 2004): 637–43. http://dx.doi.org/10.1017/s0952523804214122.

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The conventional view that glucose is the substrate for neuronal energy metabolism has been recently challenged by the “lactate shuttle” hypothesis in which glutamate cycling in glial cells drives all neuronal glucose metabolism. According to this view, glutamate released by activated retinal neurons is transported into Müller (glial) cells where it triggers glycolysis. The lactate released by Müller cells serves as the energy substrate for neuronal metabolism. Because the L-Glutamate/aspartate transporter (GLAST) is the predominant, Na+-dependent, glutamate transporter expressed by Müller cel

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3

Fujita, Hiroko, Kohji Sato, Tong-Chun Wen, Yi Peng, and Masahiro Sakanaka. "Differential Expressions of Glycine Transporter 1 and Three Glutamate Transporter mRNA in the Hippocampus of Gerbils with Transient Forebrain Ischemia." Journal of Cerebral Blood Flow & Metabolism 19, no. 6 (June 1999): 604–15. http://dx.doi.org/10.1097/00004647-199906000-00003.

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The extracellular concentrations of glutamate and its co-agonist for the N-methyl-d-aspartate (NMDA) receptor, glycine, may be under the control of amino acid transporters in the ischemic brain, However, there is little information on changes in glycine and glutamate transporters in the hippocampal CA1 field of gerbils with transient forebrain ischemia. This study investigated the spatial and temporal expressions of glycine transporter 1 (GLYT 1) and three glutamate transporter (excitatory amino acid carrier 1, EAAC 1; glutamate/aspartate transporter, GLAST; glutamate transporter 1, GLT1) mRNA

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4

Hernández-Melchor, Dinorah, Leticia Ramírez-Martínez, Luis Cid, Cecilia Palafox-Gómez, Esther López-Bayghen, and Arturo Ortega. "EAAT1-dependent slc1a3 Transcriptional Control depends on the Substrate Translocation Process." ASN Neuro 14 (January 2022): 175909142211165. http://dx.doi.org/10.1177/17590914221116574.

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Glutamate, the major excitatory neurotransmitter in the vertebrate brain, is removed from the synaptic cleft by a family of sodium-dependent transporters expressed in neurons and glial cells. The bulk of glutamate uptake activity occurs in glial cells through the sodium-dependent glutamate/aspartate transporter (EAAT1/GLAST) and glutamate transporter 1 (EAAT2/GLT-1). EAAT1/GLAST is the predominant transporter within the cerebellum. It is highly enriched in Bergmann glial cells that span the cerebellar cortex and wrap the most abundant glutamatergic synapses in the central nervous system, the s

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5

TAMAHARA, Satoshi, Mutsumi INABA, Kota SATO, Naoaki MATSUKI, Yoshiaki HIKASA, and Ken-ichiro ONO. "Non-essential roles of cysteine residues in functional expression and redox regulatory pathways for canine glutamate/aspartate transporter based on mutagenic analysis." Biochemical Journal 367, no. 1 (October 1, 2002): 107–11. http://dx.doi.org/10.1042/bj20011843.

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A redox regulatory mechanism and a molecular link between oxidative and excitotoxic neurodegeneration have been postulated for high-affinity Na+-dependent glutamate transporters. In the present study, mutations were introduced at three cysteine residues in canine glutamate/aspartate transporter (GLAST) to investigate the functional significance of thiol groups in response to oxidation. Cys(-) GLAST, in which all cysteines were replaced by other amino acids, as well as other mutants with disruption of one of three cysteine residues, showed insoluble oligomer formation, which was considered to b

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6

Deng, Yu, Zhao-Fa Xu, Wei Liu, Bin Xu, Hai-Bo Yang, and Yan-Gang Wei. "Riluzole-Triggered GSH Synthesis via Activation of Glutamate Transporters to Antagonize Methylmercury-Induced Oxidative Stress in Rat Cerebral Cortex." Oxidative Medicine and Cellular Longevity 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/534705.

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Objective. This study was to evaluate the effect of riluzole on methylmercury- (MeHg-) induced oxidative stress, through promotion of glutathione (GSH) synthesis by activating of glutamate transporters (GluTs) in rat cerebral cortex.Methods. Eighty rats were randomly assigned to four groups, control group, riluzole alone group, MeHg alone group, and riluzole + MeHg group. The neurotoxicity of MeHg was observed by measuring mercury (Hg) absorption, pathological changes, and cell apoptosis of cortex. Oxidative stress was evaluated via determining reactive oxygen species (ROS), 8-hydroxy-2-deoxyg

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7

Huggett, J. F., A. Mustafa, L. O'Neal, and D. J. Mason. "The glutamate transporter GLAST-I (EAAT-I) is expressed in the plasma membrane of osteocytes and is responsive to extracellular glutamate concentration." Biochemical Society Transactions 30, no. 6 (November 1, 2002): 890–93. http://dx.doi.org/10.1042/bst0300890.

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The glutamate/aspartate transporter GLAST-1 is expressed in bone in vivo and also exists as a splice variant (GLAST-1a) in which exon 3 is excluded. Since GLAST-1 expression is regulated in bone in response to osteogenic mechanical stimuli in vivo and binding of glutamate to receptors on osteoblasts increases osteoblast number and activity in vitro, control of extracellular glutamate concentrations may be critical for balanced bone remodelling. To determine whether GLAST isoforms may act to regulate extracellular glutamate concentration in bone we investigated whether their pattern or level of

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8

Piao, Chun-Shu, Ashley L. Holloway, Sue Hong-Routson, and Mark S. Wainwright. "Depression following traumatic brain injury in mice is associated with down-regulation of hippocampal astrocyte glutamate transporters by thrombin." Journal of Cerebral Blood Flow & Metabolism 39, no. 1 (November 14, 2017): 58–73. http://dx.doi.org/10.1177/0271678x17742792.

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Depression after traumatic brain injury (TBI) is common but the mechanisms by which TBI causes depression are unknown. TBI decreases glutamate transporters GLT-1 and GLAST and allows extravasation of thrombin. We examined the effects of thrombin on transporter expression in primary hippocampal astrocytes. Application of a PAR-1 agonist caused down-regulation of GLT-1, which was prevented by inhibition of Rho kinase (ROCK). To confirm these mechanisms in vivo, we subjected mice to closed-skull TBI. Thrombin activity in the hippocampus increased one day following TBI. Seven days following TBI, e

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9

Moshrefi-Ravasdjani, Behrouz, Daniel Ziemens, Nils Pape, Marcel Färfers, and Christine Rose. "Action Potential Firing Induces Sodium Transients in Macroglial Cells of the Mouse Corpus Callosum." Neuroglia 1, no. 1 (July 3, 2018): 106–25. http://dx.doi.org/10.3390/neuroglia1010009.

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Recent work has established that glutamatergic synaptic activity induces transient sodium elevations in grey matter astrocytes by stimulating glutamate transporter 1 (GLT-1) and glutamate-aspartate transporter (GLAST). Glial sodium transients have diverse functional consequences but are largely unexplored in white matter. Here, we employed ratiometric imaging to analyse sodium signalling in macroglial cells of mouse corpus callosum. Electrical stimulation resulted in robust sodium transients in astrocytes, oligodendrocytes and NG2 glia, which were blocked by tetrodotoxin, demonstrating their d

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10

Miyazaki, Taisuke, Miwako Yamasaki, Kouichi Hashimoto, Kazuhisa Kohda, Michisuke Yuzaki, Keiko Shimamoto, Kohichi Tanaka, Masanobu Kano, and Masahiko Watanabe. "Glutamate transporter GLAST controls synaptic wrapping by Bergmann glia and ensures proper wiring of Purkinje cells." Proceedings of the National Academy of Sciences 114, no. 28 (June 27, 2017): 7438–43. http://dx.doi.org/10.1073/pnas.1617330114.

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Astrocytes regulate synaptic transmission through controlling neurotransmitter concentrations around synapses. Little is known, however, about their roles in neural circuit development. Here we report that Bergmann glia (BG), specialized cerebellar astrocytes that thoroughly enwrap Purkinje cells (PCs), are essential for synaptic organization in PCs through the action of the l-glutamate/l-aspartate transporter (GLAST). In GLAST-knockout mice, dendritic innervation by the main ascending climbing fiber (CF) branch was significantly weakened, whereas the transverse branch, which is thin and nonsy

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11

Schreiner, Alexandra E., Eric Berlinger, Julia Langer, Karl W. Kafitz, and Christine R. Rose. "Lesion-Induced Alterations in Astrocyte Glutamate Transporter Expression and Function in the Hippocampus." ISRN Neurology 2013 (September 3, 2013): 1–16. http://dx.doi.org/10.1155/2013/893605.

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Astrocytes express the sodium-dependent glutamate transporters GLAST and GLT-1, which are critical to maintain low extracellular glutamate concentrations. Here, we analyzed changes in their expression and function following a mechanical lesion in the CA1 area of organotypic hippocampal slices. 6-7 days after lesion, a glial scar had formed along the injury site, containing strongly activated astrocytes with increased GFAP and S100β immunoreactivity, enlarged somata, and reduced capability for uptake of SR101. Astrocytes in the scar’s periphery were swollen as well, but showed only moderate upr

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12

Suzuki, Keiko, Yuji Ikegaya, Sigeru Matsuura, Yoshikatsu Kanai, Hitoshi Endou, and Norio Matsuki. "Transient upregulation of the glial glutamate transporter GLAST in response to fibroblast growth factor, insulin-like growth factor and epidermal growth factor in cultured astrocytes." Journal of Cell Science 114, no. 20 (October 15, 2001): 3717–25. http://dx.doi.org/10.1242/jcs.114.20.3717.

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Although expression of the glial glutamate transporter GLAST is tightly regulated during development and under pathophysiological conditions, little is known about endogenous modulators of GLAST expression. Because growth factors are generally believed to regulate glial functions, we addressed their possible contribution to GLAST regulation in cultured rat astrocytes. Of the six growth factors tested (basic fibroblast growth factor (bFGF), insulin-like growth factor-1 (IGF-1), epidermal growth factor (EGF), insulin, platelet-derived growth factor, and hepatocyte growth factor), bFGF, IGF-1 and

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13

Gegelashvili, Georgi, Gianluca Civenni, Giorgio Racagni, Niels C. Danbolt, Inger Schousboe, and Arne Schousboe. "Glutamate receptor agonists up-regulate glutamate transporter GLAST in astrocytes." NeuroReport 8, no. 1 (December 1996): 261–65. http://dx.doi.org/10.1097/00001756-199612200-00052.

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14

Kim, Ha-Neui, Yu-Ri Kim, Ji-Yeon Jang, Hwa-Kyoung Shin, and Byung-Tae Choi. "Electroacupuncture Confers Antinociceptive Effects via Inhibition of Glutamate Transporter Downregulation in Complete Freund's Adjuvant-Injected Rats." Evidence-Based Complementary and Alternative Medicine 2012 (2012): 1–11. http://dx.doi.org/10.1155/2012/643973.

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When we evaluated changes of glial fibrillary acidic protein (GFAP) and two glutamate transporter (GTs) by immunohistochemistry, expression of GFAP showed a significant increase in complete Freund's adjuvant (CFA)-injected rats; however, this expression was strongly inhibited by electroacupuncture (EA) stimulation. Robust downregulation of glutamate-aspartate transporter (GLAST) and glutamate transporter-1 (GLT-1) was observed in CFA-injected rats; however, EA stimulation resulted in recovery of this expression. Double-labeling staining showed co-localization of a large proportion of GLAST or

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15

Gonome, Takayuki, Yuting Xie, Saeko Arai, Kodai Yamauchi, Natsuki Maeda-Monai, Reiko Tanabu, Takashi Kudo, and Mitsuru Nakazawa. "Excess Glutamate May Cause Dilation of Retinal Blood Vessels in Glutamate/Aspartate Transporter-Deficient Mice." BioMed Research International 2019 (November 11, 2019): 1–11. http://dx.doi.org/10.1155/2019/6512195.

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Purpose. To investigate the longitudinal findings of fundus features and spectral-domain optical coherence tomography (SD-OCT) to characterize the morphologic features in a mouse model of defective glutamate/aspartate transporter (GLAST−/− mice). Materials and Methods. The fundus findings and SD-OCT images were longitudinally recorded at five time points from postnatal (P) 22 to P156 in GLAST−/− mice. As a control wild type, age-matched C57BL/6J mice were employed. The mouse retina was subdivided into five layers, and the thickness of each layer was longitudinally measured by InSight® using SD

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16

Potapenko, Evgeniy S., Vinicia C. Biancardi, Yiqiang Zhou, and Javier E. Stern. "Altered astrocyte glutamate transporter regulation of hypothalamic neurosecretory neurons in heart failure rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 303, no. 3 (August 1, 2012): R291—R300. http://dx.doi.org/10.1152/ajpregu.00056.2012.

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Neurohumoral activation, which includes augmented plasma levels of the neurohormone vasopressin (VP), is a common finding in heart failure (HF) that contributes to morbidity and mortality in this disease. While an increased activation of magnocellular neurosecretory cells (MNCs) and enhanced glutamate function in HF is well documented, the precise underlying mechanisms remain to be elucidated. Here, we combined electrophysiology and protein measurements to determine whether altered glial glutamate transporter function and/or expression occurs in the hypothalamic supraoptic nucleus (SON) during

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17

Tsuru, Noriko, Yuto Ueda, and Taku Doi. "Amygdaloid Kindling in Glutamate Transporter (GLAST) Knockout Mice." Epilepsia 43, no. 8 (August 2002): 805–11. http://dx.doi.org/10.1046/j.1528-1157.2002.36601.x.

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18

WANG, ZHIQING, WEI LI, CHERYL K. MITCHELL, and LOUVENIA CARTER-DAWSON. "Activation of protein kinase C reduces GLAST in the plasma membrane of rat Müller cells in primary culture." Visual Neuroscience 20, no. 6 (November 2003): 611–19. http://dx.doi.org/10.1017/s0952523803206039.

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In this study, a Müller cell culture preparation from young rats was used to investigate the regulation of GLAST transport activity in native cells. Immunohistochemical analysis confirmed GLAST to be the predominant glutamate transporter expressed by the cells through five passages. [3H]-glutamate uptake assays showed the typical Na+-dependent glutamate transport which was blocked by L-(-)-threo-3-hydroxyaspartate (L-THA), a competitive inhibitor. Glutamate transport was decreased significantly in Müller cells exposed to phorbol-12-myristate-13-acetate (PMA), a protein kinase C (PKC) activator

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19

Lin, Chia-Ho, Han-Yu Chen, and Kai-Che Wei. "Role of HMGB1/TLR4 Axis in Ischemia/Reperfusion-Impaired Extracellular Glutamate Clearance in Primary Astrocytes." Cells 9, no. 12 (December 3, 2020): 2585. http://dx.doi.org/10.3390/cells9122585.

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(1) Background: Abnormal accumulation of extracellular glutamate can occur as dysfunction of astrocytic glutamate transporters, which has been linked to ischemic brain injury. Excessive extracellular glutamate-induced abnormal excitotoxicity is the major cause of secondary neuronal damage after cerebral ischemia/reperfusion. However, the definite mechanism of impaired astrocytic glutamate reuptake remains unclear. (2) Methods: We investigated the mechanism of the HMGB1/TLR4 axis in extracellular glutamate clearance in primary astrocytes exposed to ischemia/reperfusion by using OGD/R (oxygen-gl

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20

FYK-KOLODZIEJ, BOZENA, PU QIN, ARTURIK DZHAGARYAN, and ROBERTA G. POURCHO. "Differential cellular and subcellular distribution of glutamate transporters in the cat retina." Visual Neuroscience 21, no. 4 (July 2004): 551–65. http://dx.doi.org/10.1017/s0952523804214067.

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Retrieval of glutamate from extracellular sites in the retina involves at least five excitatory amino acid transporters. Immunocytochemical analysis of the cat retina indicates that each of these transporters exhibits a selective distribution which may reflect its specific function. The uptake of glutamate into Müller cells or astrocytes appears to depend upon GLAST and EAAT4, respectively. Staining for EAAT4 was also seen in the pigment epithelium. The remaining transporters are neuronal with GLT-1α localized to a number of cone bipolar, amacrine, and ganglion cells and GLT-1v in cone photore

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21

Wahle, S., and W. Stoffel. "Membrane topology of the high-affinity L-glutamate transporter (GLAST-1) of the central nervous system." Journal of Cell Biology 135, no. 6 (December 15, 1996): 1867–77. http://dx.doi.org/10.1083/jcb.135.6.1867.

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The membrane topology of the high affinity, Na(+)-coupled L-glutamate/L-aspartate transporter (GLAST-1) of the central nervous system has been determined. Truncated GLAST-1 cDNA constructs encoding protein fragments with an increasing number of hydrophobic regions were fused to a cDNA encoding a reporter peptide with two N-glycosylation sites. The respective cRNA chimeras were translated in vitro and in vivo in Xenopus oocytes. Posttranslational N-glycosylation of the two reporter consensus sites monitors the number, size, and orientation of membrane-spanning domains. The results of our experi

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Wakabayashi, Maki, Toshio Hasegawa, Takuji Yamaguchi, Naoko Funakushi, Hajime Suto, Rie Ueki, Hiroyuki Kobayashi, Hideoki Ogawa, and Shigaku Ikeda. "Yokukansan, a Traditional Japanese Medicine, Adjusts Glutamate Signaling in Cultured Keratinocytes." BioMed Research International 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/364092.

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Glutamate plays an important role in skin barrier signaling. In our previous study, Yokukansan (YKS) affected glutamate receptors in NC/Nga mice and was ameliorated in atopic dermatitis lesions. The aim of this study was to assess the effect of YKS on skin and cultured human keratinocytes. Glutamate concentrations in skin of YKS-treated and nontreated NC/Nga mice were measured. Then, glutamate release from cultured keratinocytes was measured, and extracellular glutamate concentrations in YKS-stimulated cultured human keratinocytes were determined. The mRNA expression levels of NMDA receptor 2D

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23

Suzuki, Gentaroh, Hiroshi Kawamoto та Hisashi Ohta. "Development of a β-Lactamase Reporter Gene Assay for Metabotropic Glutamate Receptor 1 by Using Coexpression of Glutamate Transporter". Journal of Biomolecular Screening 15, № 2 (19 січня 2010): 148–58. http://dx.doi.org/10.1177/1087057109356982.

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mGluR1 antagonists have been postulated to be novel CNS drugs, including antipsychotics. Toward this end, the authors developed a β-lactamase reporter assay to identify mGluR1 antagonists. β-Lactamase has several interesting features for high-throughput screening, including very high sensitivity and less well-to-well variation than other reporter enzymes. mGluR1-expressing Chinese hamster ovary (CHO) cells with the β-lactamase gene under control of the nuclear factor of activated T cells (NFAT) promoter (CHO-NFAT-bla-hmGluR1b) exhibited very high basal activity, resulting in an inadequate sign

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Yu, Jun, Yan Yan, Yiye Chen, Yan Zheng, Xiaoyan Yu, Jialu Wang, Yafu Wang, et al. "A2AR Antagonists Upregulate Expression of GS and GLAST in Rat Hypoxia Model." BioMed Research International 2020 (October 26, 2020): 1–8. http://dx.doi.org/10.1155/2020/2054293.

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Background. The aim of this study was to research the effects of glutamine synthetase (GS) and glutamate aspartate transporter (GLAST) in rat Müller cells and the effects of an adenosine A2AR antagonist (SCH 442416) on GS and GLAST in hypoxia both in vivo and in vitro. Methods. This study used RT-PCR and Western blotting to quantify the expressions of GS and GLAST under different hypoxic conditions as well as the expressions of GS and GLAST at different drug concentrations. A cell viability assay was used to assess drug toxicity. Results. mRNA and protein expression of GS and GLAST in hypoxia

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Namekata, Kazuhiko, Chikako Harada, Kuniko Kohyama, Yoh Matsumoto, and Takayuki Harada. "Interleukin-1 Stimulates Glutamate Uptake in Glial Cells by Accelerating Membrane Trafficking of Na+/K+-ATPase via Actin Depolymerization." Molecular and Cellular Biology 28, no. 10 (March 10, 2008): 3273–80. http://dx.doi.org/10.1128/mcb.02159-07.

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ABSTRACT Interleukin-1 (IL-1) is a mediator of brain injury induced by ischemia, trauma, and chronic neurodegenerative disease. IL-1 also has a protective role by preventing neuronal cell death from glutamate neurotoxicity. However, the cellular mechanisms of IL-1 action remain unresolved. In the mammalian retina, glutamate/aspartate transporter (GLAST) is a Na+-dependent, major glutamate transporter localized to Müller glial cells, and loss of GLAST leads to glaucomatous retinal degeneration (T. Harada, C. Harada, K. Nakamura, H. A. Quah, A. Okumura, K. Namekata, T. Saeki, M. Aihara, H. Yosh

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Dąbrowska-Bouta, Beata, Grzegorz Sulkowski, Mikołaj Sałek, Magdalena Gewartowska, Marta Sidoryk-Węgrzynowicz, and Lidia Strużyńska. "Early Postnatal Exposure to a Low Dose of Nanoparticulate Silver Induces Alterations in Glutamate Transporters in Brain of Immature Rats." International Journal of Molecular Sciences 21, no. 23 (November 26, 2020): 8977. http://dx.doi.org/10.3390/ijms21238977.

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Due to strong antimicrobial properties, silver nanoparticles (AgNPs) are used in a wide range of medical and consumer products, including those dedicated for infants and children. While AgNPs are known to exert neurotoxic effects, current knowledge concerning their impact on the developing brain is scarce. During investigations of mechanisms of neurotoxicity in immature rats, we studied the influence of AgNPs on glutamate transporter systems which are involved in regulation of extracellular concentration of glutamate, an excitotoxic amino acid, and compared it with positive control—Ag citrate.

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Ueki, Toshiyuki, Zenji Kawakami, Hitomi Kanno, Yuji Omiya, Kazushige Mizoguchi, and Masahiro Yamamoto. "Yokukansan, a Traditional Japanese Medicine, Enhances the Glutamate Transporter GLT-1 Function in Cultured Rat Cortical Astrocytes." Evidence-Based Complementary and Alternative Medicine 2018 (2018): 1–9. http://dx.doi.org/10.1155/2018/6804017.

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Astrocytes carry two glutamate transporters—GLAST and GLT-1—the latter of which is responsible for >90% of glutamate uptake activity in the brain; however, under culture conditions, the GLT-1 expression in astrocytes is exceedingly low, as is the glutamate uptake activity mediated by GLT-1. This study aimed to elucidate the effects of yokukansan (YKS) in relation to the GLT-1-mediated regulation of extracellular glutamate concentrations. Thus, we treated cultured astrocytes with tumor necrosis factor-α (TNF-α) and dibutyryl-cAMP (dBcAMP) (hereinafter, referred to as “TA”) to increase GLT-1

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Bauer, Deborah E., Joshua G. Jackson, Elizabeth N. Genda, Misty M. Montoya, Marc Yudkoff, and Michael B. Robinson. "The glutamate transporter, GLAST, participates in a macromolecular complex that supports glutamate metabolism." Neurochemistry International 61, no. 4 (September 2012): 566–74. http://dx.doi.org/10.1016/j.neuint.2012.01.013.

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Jin, Zhen-Hua, Toshihiko Kikuchi, Kohichi Tanaka, and Toshimitsu Kobayashi. "Expression of Glutamate Transporter GLAST in the Developing Mouse Cochlea." Tohoku Journal of Experimental Medicine 200, no. 3 (2003): 137–44. http://dx.doi.org/10.1620/tjem.200.137.

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Zhou, Bo-Guang, and Michael D. Norenberg. "Ammonia downregulates GLAST mRNA glutamate transporter in rat astrocyte cultures." Neuroscience Letters 276, no. 3 (December 1999): 145–48. http://dx.doi.org/10.1016/s0304-3940(99)00816-2.

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31

Niederberger, Ellen, Achim Schmidtko, Ovidiu Coste, Claudiu Marian, Corina Ehnert, and Gerd Geisslinger. "The glutamate transporter GLAST is involved in spinal nociceptive processing." Biochemical and Biophysical Research Communications 346, no. 2 (July 2006): 393–99. http://dx.doi.org/10.1016/j.bbrc.2006.05.163.

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Lehre, Knut P., Svend Davanger, and Niels C. Danbolt. "Localization of the glutamate transporter protein GLAST in rat retina." Brain Research 744, no. 1 (January 1997): 129–37. http://dx.doi.org/10.1016/s0006-8993(96)01022-0.

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Chen, Xiaomin, Yue Wang, Fangfang Han, and Min Ke. "Cyanin Chloride Inhibits Hyperbaric Pressure-Induced Decrease of Intracellular Glutamate-Aspartate Transporter in Rat Retinal Müller Cells." Journal of Ophthalmology 2018 (October 31, 2018): 1–6. http://dx.doi.org/10.1155/2018/6128470.

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Purpose. Glaucoma is the leading cause of irreversible blindness throughout the world. The pathogenesis of glaucoma is complex, and neuroprotection is a crucial aspect of therapy. High concentrations of extracellular glutamate are toxic to the optic nerve. The glutamate-aspartate transporter (GLAST) in retinal Müller cells is involved in the development of glaucoma. Anthocyanin has been reported to protect retinal neurons. We hypothesize that cyanin chloride, a type of anthocyanin, can inhibit hyperbaric pressure-induced GLAST decreases in cultured rat retinal Müller cells and may serve as a p

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Cholet, Nathalie, Luc Pellerin, Egbert Welker, Pierre Lacombe, Jacques Seylaz, Pierre Magistretti, and Gilles Bonvento. "Local Injection of Antisense Oligonucleotides Targeted to the Glial Glutamate Transporter GLAST Decreases the Metabolic Response to Somatosensory Activation." Journal of Cerebral Blood Flow & Metabolism 21, no. 4 (April 2001): 404–12. http://dx.doi.org/10.1097/00004647-200104000-00009.

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The mechanisms responsible for the local increase in brain glucose utilization during functional activation remain unknown. Recent in vitro studies have identified a new signaling pathway involving an activation of glial glutamate transporters and enhancement of neuron–astrocyte metabolic interactions that suggest a putative coupling mechanism. The aim of the present study was to determine whether one of the glutamate transporters exclusively expressed in astrocytes, GLAST, is involved in the neurometabolic coupling in vivo. For this purpose, rats were microinjected into the posteromedial barr

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Lawton, D. Maxwell, David N. Furness, Bernd Lindemann, and Carole M. Hackney. "Localization of the glutamate-aspartate transporter, GLAST, in rat taste buds." European Journal of Neuroscience 12, no. 9 (September 2000): 3163–71. http://dx.doi.org/10.1046/j.1460-9568.2000.00207.x.

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36

Gottlieb, M., M. Domercq, and C. Matute. "Altered Expression of the Glutamate Transporter EAAC1 in Neurons and Immature Oligodendrocytes after Transient Forebrain Ischemia." Journal of Cerebral Blood Flow & Metabolism 20, no. 4 (April 2000): 678–87. http://dx.doi.org/10.1097/00004647-200004000-00005.

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Glutamate uptake is reduced during ischemia because of perturbations of ionic gradients across neuronal and glial membranes. Using immunohistochemical and Western blot analyses, the authors examined the expression of the glutamate transporters EAAC1, GLAST, and GLT-1 in the rat hippocampus and cerebral cortex 8 hours and 1 to 28 days after transient forebrain ischemia. Densitometric analysis of immunoblots of CA1 homogenates showed a moderate increase in EAAC1 protein levels early after the insult. Consistently, it was observed that EAAC1 immunostaining in CA1 pyramidal neurons was more intens

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Masocha, Willias. "Astrocyte activation in the anterior cingulate cortex and altered glutamatergic gene expression during paclitaxel-induced neuropathic pain in mice." PeerJ 3 (October 22, 2015): e1350. http://dx.doi.org/10.7717/peerj.1350.

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Spinal astrocyte activation contributes to the pathogenesis of paclitaxel-induced neuropathic pain (PINP) in animal models. We examined glial fibrillary acidic protein (GFAP; an astrocyte marker) immunoreactivity and gene expression of GFAP, glutamate transporters and receptor subunits by real time PCR in the anterior cingulate cortex (ACC) at 7 days post first administration of paclitaxel, a time point when mice had developed thermal hyperalgesia. The ACC, an area in the brain involved in pain perception and modulation, was chosen because changes in this area might contribute to the pathophys

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Sun, Dong, Zhi-Bing Tan, Xiang-Dong Sun, Zhi-Peng Liu, Wen-Bing Chen, Leena Milibari, Xiao Ren, et al. "Hippocampal astrocytic neogenin regulating glutamate uptake, a critical pathway for preventing epileptic response." Proceedings of the National Academy of Sciences 118, no. 16 (April 13, 2021): e2022921118. http://dx.doi.org/10.1073/pnas.2022921118.

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Epilepsy, a common neurological disorder, is featured with recurrent seizures. Its underlying pathological mechanisms remain elusive. Here, we provide evidence for loss of neogenin (NEO1), a coreceptor for multiple ligands, including netrins and bone morphological proteins, in the development of epilepsy. NEO1 is reduced in hippocampi from patients with epilepsy based on transcriptome and proteomic analyses. Neo1 knocking out (KO) in mouse brains displays elevated epileptiform spikes and seizure susceptibility. These phenotypes were undetectable in mice, with selectively depleted NEO1 in excit

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Leonova, Julia, Thorleif Thorlin, N. David Åberg, Peter S. Eriksson, Lars Rönnbäck, and Elisabeth Hansson. "Endothelin-1 decreases glutamate uptake in primary cultured rat astrocytes." American Journal of Physiology-Cell Physiology 281, no. 5 (November 1, 2001): C1495—C1503. http://dx.doi.org/10.1152/ajpcell.2001.281.5.c1495.

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Endothelin-1 (ET-1) is a potent vasoconstrictor peptide that is also known to induce a wide spectrum of biological responses in nonvascular tissue. In this study, we found that ET-1 (100 nM) inhibited the glutamate uptake in cultured astrocytes expressing the glutamate/aspartate transporter (GLAST); astrocytes did not express the glutamate transporter-1 (GLT-1). The V maxand the K m of the glutamate uptake were reduced by 57% and 47%, respectively. Application of the ETA and ETB receptor antagonists BQ-123 and BQ-788 partly inhibited the ET-1-evoked decrease in the glutamate uptake, whereas th

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Owe, Simen Gylterud, Païkan Marcaggi, and David Attwell. "The ionic stoichiometry of the GLAST glutamate transporter in salamander retinal glia." Journal of Physiology 577, no. 2 (November 24, 2006): 591–99. http://dx.doi.org/10.1113/jphysiol.2006.116830.

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Watanabe, Takemi, Kiyoshi Morimoto, Toru Hirao, Hiroshi Suwaki, Kei Watase, and Kohichi Tanaka. "Amygdala-kindled and pentylenetetrazole-induced seizures in glutamate transporter GLAST-deficient mice." Brain Research 845, no. 1 (October 1999): 92–96. http://dx.doi.org/10.1016/s0006-8993(99)01945-9.

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Watanabe, Takemi, Kiyoshi Morimoto, Toru Hirao, Hiroshi Suwaki, Kei Watase, and Kohi chi Tanaka. "Amygdala-Kindling and Pentylenetetrazole-Induced Seizures in Glutamate Transporter GLAST-Deficient Mice." Epilepsia 41, s9 (September 2000): 49–50. http://dx.doi.org/10.1111/j.1528-1157.2000.tb02222.x.

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Matsuura, Sigeru, Yuji Ikegaya, Maki K. Yamada, Nobuyoshi Nishiyama, and Norio Matsuki. "Endothelin downregulates the glutamate transporter GLAST in cAMP-differentiated astrocytes in vitro." Glia 37, no. 2 (December 19, 2001): 178–82. http://dx.doi.org/10.1002/glia.10020.

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Dematteis, Giulia, Elena Restelli, Roberto Chiesa, Eleonora Aronica, Armando A. Genazzani, Dmitry Lim, and Laura Tapella. "Calcineurin Controls Expression of EAAT1/GLAST in Mouse and Human Cultured Astrocytes through Dynamic Regulation of Protein Synthesis and Degradation." International Journal of Molecular Sciences 21, no. 6 (March 23, 2020): 2213. http://dx.doi.org/10.3390/ijms21062213.

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Alterations in the expression of glutamate/aspartate transporter (GLAST) have been associated with several neuropathological conditions including Alzheimer’s disease and epilepsy. However, the mechanisms by which GLAST expression is altered are poorly understood. Here we used a combination of pharmacological and genetic approaches coupled with quantitative PCR and Western blot to investigate the mechanism of the regulation of GLAST expression by a Ca2+/calmodulin-activated phosphatase calcineurin (CaN). We show that treatment of cultured hippocampal mouse and fetal human astrocytes with a CaN

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Erikson, Keith, and Michael Aschner. "Manganese Causes Differential Regulation of Glutamate Transporter (GLAST) Taurine Transporter and Metallothionein in Cultured Rat Astrocytes." NeuroToxicology 23, no. 4-5 (October 2002): 595–602. http://dx.doi.org/10.1016/s0161-813x(02)00012-8.

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Rauen, T., W. Rowland Taylor, Kirsten Kuhlbrodt, and Michael Wiessner. "High-affinity glutamate transporters in the rat retina: a major role of the glial glutamate transporter GLAST-1 in transmitter clearance." Cell and Tissue Research 291, no. 1 (December 12, 1997): 19–31. http://dx.doi.org/10.1007/s004410050976.

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Kashem, Mohammed Abul, Omar Šerý, David V. Pow, Benjamin D. Rowlands, Caroline D. Rae, and Vladimir J. Balcar. "Actions of Alcohol in Brain: Genetics, Metabolomics, GABA Receptors, Proteomics and Glutamate Transporter GLAST/EAAT1." Current Molecular Pharmacology 14, no. 2 (December 31, 2020): 138–49. http://dx.doi.org/10.2174/1874467213666200424155244.

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We present an overview of genetic, metabolomic, proteomic and neurochemical studies done mainly in our laboratories that could improve prediction, mechanistic understanding and possibly extend to diagnostics and treatment of alcoholism and alcohol addiction. Specific polymorphisms in genes encoding for interleukins 2 and 6, catechol-O-methyl transferase (COMT), monaminooxidase B (MAO B) and several other enzymes were identified as associated with altered risks of alcoholism in humans. A polymorphism in the gene for BDNF has been linked to the risk of developing deficiences in colour vision som

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Gegelashvili, Marina, Anna Rodriguez-Kern, Iryna Pirozhkova, Jian Zhang, Luther Sung, and Georgi Gegelashvili. "High-affinity glutamate transporter GLAST/EAAT1 regulates cell surface expression of glutamine/neutral amino acid transporter ASCT2 in human fetal astrocytes." Neurochemistry International 48, no. 6-7 (May 2006): 611–15. http://dx.doi.org/10.1016/j.neuint.2005.12.033.

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Hakuba, Nobuhiro, Kenichiro Koga, Kiyofumi Gyo, Shin-ichi Usami, and Kohichi Tanaka. "Exacerbation of Noise-Induced Hearing Loss in Mice Lacking the Glutamate Transporter GLAST." Journal of Neuroscience 20, no. 23 (December 1, 2000): 8750–53. http://dx.doi.org/10.1523/jneurosci.20-23-08750.2000.

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Kinoshita, Nagatoki, Kazushi Kimura, Naoya Matsumoto, Masahiko Watanabe, Masahiro Fukaya, and Chizuka Ide. "Mammalian septin Sept2 modulates the activity of GLAST, a glutamate transporter in astrocytes." Genes to Cells 9, no. 1 (January 2004): 1–14. http://dx.doi.org/10.1111/j.1356-9597.2004.00696.x.

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