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Gotowe bibliografie tematyczne / Glutamate transporter GLAST

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Gotowa bibliografia na temat „Glutamate transporter GLAST”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 21 lutego 2023

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Artykuły w czasopismach na temat "Glutamate transporter GLAST"

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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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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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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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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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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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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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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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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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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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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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Rozprawy doktorskie na temat "Glutamate transporter GLAST"

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Kinoshita, Nagatoki. "Mammalian septin Sept2 modulates the activity of GLAST, a glutamate transporter in astrocytes." Kyoto University, 2004. http://hdl.handle.net/2433/147473.

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Nguyen, Khoa Thuy Diem. "Energy metabolism in the brain and rapid distribution of glutamate transporter GLAST in astrocytes." Thesis, The University of Sydney, 2008. http://hdl.handle.net/2123/3996.

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Glutamate transporters play a role in removing extracellular excitatory neurotransmitter, L-glutamate into the cells. The rate of the uptake depends on the density of the transporters at the membrane. Some studies claimed that glutamate transporters could transit between the cytoplasm and the membrane on a time-scale of minutes. The present study examined the distribution of glutamate transporter GLAST predominantly expressed in rat cortical cultured astrocytes between the membrane and the cytoplasm by using deconvolution microscopy and then analyzing the images. The regulation of the dist

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Nguyen, Khoa Thuy Diem. "Energy metabolism in the brain and rapid distribution of glutamate transporter GLAST in astrocytes." University of Sydney, 2008. http://hdl.handle.net/2123/3996.

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Doctor of Philosophy (Medicine)<br>Glutamate transporters play a role in removing extracellular excitatory neurotransmitter, L-glutamate into the cells. The rate of the uptake depends on the density of the transporters at the membrane. Some studies claimed that glutamate transporters could transit between the cytoplasm and the membrane on a time-scale of minutes. The present study examined the distribution of glutamate transporter GLAST predominantly expressed in rat cortical cultured astrocytes between the membrane and the cytoplasm by using deconvolution microscopy and then analyzing the

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Hulme, Julie Anne. "Ultrastructural and immunocytochemical studies of the glutamate/aspartate transporter, GLAST, and its relationship to glutamate handling in the mammalian cochlea." Thesis, Keele University, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.401057.

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Meyer, Logan. "Novel Role of the Nociceptin System as a Regulator of Glutamate Transporter Expression in Developing Astrocytes." VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4931.

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Our previous results showed that oligodendrocyte development is regulated by both nociceptin and its G-protein coupled receptor, the nociceptin/orphanin FQ receptor (NOPR). The present in vitro and in vivo findings show that nociceptin plays a crucial conserved role in both human and rodent brain astrocytes, regulating the levels of the glutamate/aspartate transporter GLAST/EAAT1. This nociceptin-mediated response takes place during a critical developmental window that coincides with astrocyte maturation and synapse formation. GLAST/EAAT1 upregulation by nociceptin is mediated by NOPR and the

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Alshehri, Fahad. "Role of Modulating Glutamate Transporters on Hydrocodone and Alcohol Co-Abuse inAlcohol-Preferring Rats." University of Toledo Health Science Campus / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=mco153245611012862.

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Colin, Angélique. "Développement d'un vecteur lentiviral ciblant les astrocytes et mise en application dans l'étude des transporteurs au glutamate GLAST et GLT-1." Phd thesis, Université Pierre et Marie Curie - Paris VI, 2008. http://tel.archives-ouvertes.fr/tel-00348988.

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Les astrocytes sont des cellules gliales jouant un rôle primordial dans le fonctionnement cérébral. Ils remplissent de nombreuses fonctions allant de la régulation de l'homéostasie ionique, à la modulation de la transmission synaptique en passant par la régulation du métabolisme énergétique. Les transporteurs astrocytaires au glutamate GLAST et GLT-1 tiennent un rôle particulièrement important dans ces fonctions astrocytaires. La recapture du glutamate libéré dans la synapse module la neurotransmission et évite la stimulation excessive des récepteurs glutamatergiques qui peut induire des phéno

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Colin, Angélique. "Développement d’un vecteur lentiviral ciblant les astrocytes in vivo et mise en application dans l’étude des transporteurs au glutamate GLAST et GLT-1." Paris 6, 2008. http://www.theses.fr/2008PA066423.

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Les astrocytes remplissent de nombreuses fonctions primordiales dans le cerveau notamment la modulation de la transmission synaptique et le couplage neurométabolique qui impliquent les transporteurs astrocytaires au glutamate GLAST et GLT-1. Leur étude est essentielle, cependant, il existe peu d’outils permettant l’étude de leur fonction in vivo. Notre objectif a été de développer un nouveau vecteur lentiviral permettant un transfert de gène uniquement dans les astrocytes in vivo. Nous avons développé trois voies de recherche : le changement de l’enveloppe du vecteur, du promoteur et une nouve

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SATO, Kota. "Molecular Pathobiological Studies on Glutamate/Aspartate Transporter (GLAST) in Canine Red Cells : Molecular Basis for Hereditary Deficiency of GLAST in Dogs." Doctoral thesis, 2000. http://hdl.handle.net/2115/28086.

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Części książek na temat "Glutamate transporter GLAST"

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Tserga, Evangelia, Peter Damberg, Barbara Canlon, and Christopher R. Cederroth. "Auditory synaptopathy in mice lacking the glutamate transporter GLAST and its impact on brain activity." In Progress in Brain Research. Elsevier, 2020. http://dx.doi.org/10.1016/bs.pbr.2020.04.004.

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