Log in

Relevant bibliographies by topics / Transporteur de glutamate / Journal articles

To see the other types of publications on this topic, follow the link: Transporteur de glutamate.

Journal articles on the topic 'Transporteur de glutamate'

Author: Grafiati

Published: 4 June 2021

Last updated: 17 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Transporteur de glutamate.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Henderson, Fiona, Vincent Vialou, Salah El Mestikawy, and Veronique Fabre. "Régulation du sommeil par les neurones exprimant le transporteur vésiculaire du glutamate de type 3 (VGLUT3)." Médecine du Sommeil 13, no. 1 (2016): 48. http://dx.doi.org/10.1016/j.msom.2016.01.044.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Welbourne, T. C., and D. Chevalier. "Glutamate transport and not cellular content modulates paracellular permeability in LLC-PK1-F+ cells." American Journal of Physiology-Endocrinology and Metabolism 272, no. 3 (1997): E367—E370. http://dx.doi.org/10.1152/ajpendo.1997.272.3.e367.

Full text

Abstract:

Uptake of glutamate modulates two cellular processes: 1) glutamine flux through the cellular glutaminase (GA) and 2) paracellular permeability (PP). Because both responses are the result of a decreased glutamate uptake, the present study was designed to determine whether the transport step or resulting fall in cellular glutamate modulates PP. To do so, advantage was taken of the ability of D-glutamate to competitively displace the natural L-isomer yet maintain transporter activity at or even above that normally occurring with L-glutamate. As a consequence cellular L-glutamate would fall while

APA, Harvard, Vancouver, ISO, and other styles

3

Zhou, Yun, Leonie F. Waanders, Silvia Holmseth, et al. "Proteome Analysis and Conditional Deletion of the EAAT2 Glutamate Transporter Provide Evidence against a Role of EAAT2 in Pancreatic Insulin Secretion in Mice." Journal of Biological Chemistry 289, no. 3 (2013): 1329–44. http://dx.doi.org/10.1074/jbc.m113.529065.

Full text

Abstract:

Islet function is incompletely understood in part because key steps in glutamate handling remain undetermined. The glutamate (excitatory amino acid) transporter 2 (EAAT2; Slc1a2) has been hypothesized to (a) provide islet cells with glutamate, (b) protect islet cells against high extracellular glutamate concentrations, (c) mediate glutamate release, or (d) control the pH inside insulin secretory granules. Here we floxed the EAAT2 gene to produce the first conditional EAAT2 knock-out mice. Crossing with Nestin-cyclization recombinase (Cre) eliminated EAAT2 from the brain, resulting in epilepsy

APA, Harvard, Vancouver, ISO, and other styles

4

BRÖER, Angelika, Carsten A. WAGNER, Florian LANG, and Stefan BRÖER. "The heterodimeric amino acid transporter 4F2hc/y+LAT2 mediates arginine efflux in exchange with glutamine." Biochemical Journal 349, no. 3 (2000): 787–95. http://dx.doi.org/10.1042/bj3490787.

Full text

Abstract:

The cationic amino acid arginine, due to its positive charge, is usually accumulated in the cytosol. Nevertheless, arginine has to be released by a number of cell types, e.g. kidney cells, which supply other organs with this amino acid, or the endothelial cells of the blood–brain barrier which release arginine into the brain. Arginine release in mammalian cells can be mediated by two different transporters, y+LAT1 and y+LAT2. For insertion into the plasma membrane, these transporters have to be associated with the type-II membrane glycoprotein 4F2hc [Torrents, Estevez, Pineda, Fernandez, Llobe

APA, Harvard, Vancouver, ISO, and other styles

5

Henderson, Fiona, Salah El Mestikawy, and Véronique Fabre. "Régulation du sommeil et de l’anxiété par les neurones exprimant le transporteur vésiculaire du glutamate de type 3 (VGLUT3)." Médecine du Sommeil 14, no. 1 (2017): 57. http://dx.doi.org/10.1016/j.msom.2017.01.004.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Porcheray, Fabrice, Cathie Léone, Boubekeur Samah, Anne-Cécile Rimaniol, Nathalie Dereuddre-Bosquet, and Gabriel Gras. "Glutamate metabolism in HIV-infected macrophages: implications for the CNS." American Journal of Physiology-Cell Physiology 291, no. 4 (2006): C618—C626. http://dx.doi.org/10.1152/ajpcell.00021.2006.

Full text

Abstract:

Central nervous system disorders are still a common complication of human immunodeficiency virus (HIV) infection and can lead to dementia and death. They are mostly the consequences of an inflammatory macrophagic activation and relate to glutamate-mediated excitotoxicity. However, recent studies also suggest neuroprotective aspects of macrophage activation through the expression of glutamate transporters and glutamine synthetase. We thus aimed to study whether HIV infection or activation of macrophages could modulate glutamate metabolism in these cells. We assessed the effect of HIV infection

APA, Harvard, Vancouver, ISO, and other styles

7

Shim, Myoung Sup, Jin Young Kim, Kwang Hee Lee, et al. "l(2)01810 is a novel type of glutamate transporter that is responsible for megamitochondrial formation." Biochemical Journal 439, no. 2 (2011): 277–86. http://dx.doi.org/10.1042/bj20110582.

Full text

Abstract:

l(2)01810 causes glutamine-dependent megamitochondrial formation when it is overexpressed in Drosophila cells. In the present study, we elucidated the function of l(2)01810 during megamitochondrial formation. The overexpression of l(2)01810 and the inhibition of glutamine synthesis showed that l(2)01810 is involved in the accumulation of glutamate. l(2)01810 was predicted to contain transmembrane domains and was found to be localized to the plasma membrane. By using 14C-labelled glutamate, l(2)01810 was confirmed to uptake glutamate into Drosophila cells with high affinity (Km=69.4 μM). Also,

APA, Harvard, Vancouver, ISO, and other styles

8

Vandenberg, Robert J., Cheryl A. Handford, Ewan M. Campbell, Renae M. Ryan, and Andrea J. Yool. "Water and urea permeation pathways of the human excitatory amino acid transporter EAAT1." Biochemical Journal 439, no. 2 (2011): 333–40. http://dx.doi.org/10.1042/bj20110905.

Full text

Abstract:

Glutamate transport is coupled to the co-transport of 3 Na+ and 1 H+ followed by the counter-transport of 1 K+. In addition, glutamate and Na+ binding to glutamate transporters generates an uncoupled anion conductance. The human glial glutamate transporter EAAT1 (excitatory amino acid transporter 1) also allows significant passive and active water transport, which suggests that water permeation through glutamate transporters may play an important role in glial cell homoeostasis. Urea also permeates EAAT1 and has been used to characterize the permeation properties of the transporter. We have pr

APA, Harvard, Vancouver, ISO, and other styles

9

Trip, Hein, Niels L. Mulder, and Juke S. Lolkema. "Cloning, Expression, and Functional Characterization of Secondary Amino Acid Transporters of Lactococcus lactis." Journal of Bacteriology 195, no. 2 (2012): 340–50. http://dx.doi.org/10.1128/jb.01948-12.

Full text

Abstract:

ABSTRACTFourteen genes encoding putative secondary amino acid transporters were identified in the genomes ofLactococcus lactissubsp.cremorisstrains MG1363 and SK11 andL. lactissubsp. lactisstrains IL1403 and KF147, 12 of which were common to all four strains. Amino acid uptake inL. lactiscells overexpressing the genes revealed transporters specific for histidine, lysine, arginine, agmatine, putrescine, aromatic amino acids, acidic amino acids, serine, and branched-chain amino acids. Substrate specificities were demonstrated by inhibition profiles determined in the presence of excesses of the o

APA, Harvard, Vancouver, ISO, and other styles

10

Yalçın, G. Dönmez, and M. Colak. "SIRT4 prevents excitotoxicity via modulating glutamate metabolism in glioma cells." Human & Experimental Toxicology 39, no. 7 (2020): 938–47. http://dx.doi.org/10.1177/0960327120907142.

Full text

Abstract:

Excitotoxicity is the presence of excessive glutamate, which is normally taken up by glutamate transporters on astrocytes. Glutamate transporter 1 (GLT-1) is the major transporter on glia cells clearing more than 90% of the glutamate. Sirtuin 4 (SIRT4) is a mitochondrial sirtuin which is expressed in the brain. Previously, it was shown that loss of SIRT4 leads to a more severe reaction to kainic acid, an excitotoxic agent, and also decreased GLT-1 expression in the brain. In this study, we aimed to investigate whether overexpression of SIRT4 is protective against excitotoxicity in glia cells.

APA, Harvard, Vancouver, ISO, and other styles

11

Ishikawa, Makoto. "Abnormalities in Glutamate Metabolism and Excitotoxicity in the Retinal Diseases." Scientifica 2013 (2013): 1–13. http://dx.doi.org/10.1155/2013/528940.

Full text

Abstract:

In the physiological condition, glutamate acts as an excitatory neurotransmitter in the retina. However, excessive glutamate can be toxic to retinal neurons by overstimulation of the glutamate receptors. Glutamate excess is primarily attributed to perturbation in the homeostasis of the glutamate metabolism. Major pathway of glutamate metabolism consists of glutamate uptake by glutamate transporters followed by enzymatic conversion of glutamate to nontoxic glutamine by glutamine synthetase. Glutamate metabolism requires energy supply, and the energy loss inhibits the functions of both glutamate

APA, Harvard, Vancouver, ISO, and other styles

12

Borisova, Tatiana. "Permanent dynamic transporter-mediated turnover of glutamate across the plasma membrane of presynaptic nerve terminals: arguments in favor and against." Reviews in the Neurosciences 27, no. 1 (2016): 71–81. http://dx.doi.org/10.1515/revneuro-2015-0023.

Full text

Abstract:

AbstractMechanisms for maintenance of the extracellular level of glutamate in brain tissue and its regulation still remain almost unclear, and criticism of the current paradigm of glutamate transport and homeostasis has recently appeared. The main premise for this study is the existence of a definite and non-negligible concentration of ambient glutamate between the episodes of exocytotic release in our experiments with rat brain nerve terminals (synaptosomes), despite the existence of a very potent Na+-dependent glutamate uptake. Glutamate transporter reversal is considered as the main mechani

APA, Harvard, Vancouver, ISO, and other styles

13

Hediger, M. A., and T. C. Welbourne. "Introduction: Glutamate transport, metabolism, and physiological responses." American Journal of Physiology-Renal Physiology 277, no. 4 (1999): F477—F480. http://dx.doi.org/10.1152/ajprenal.1999.277.4.f477.

Full text

Abstract:

The material covered in this set of articles was originally presented at Experimental Biology ’98, in San Francisco, CA, on April 20, 1998. Here, the participants recount important elements of current research on the role of glutamate transporter activity in cellular signaling, metabolism, and organ function. W. A. Fairman and S. G. Amara discuss the five subtypes of human excitatory amino acid transporters, with emphasis on the EAAT4 subtype. M. A. Hediger discusses the expression and action of EAAC1 subtype of the human excitatory amino acid transporter. I. Nissim provides an overview of the

APA, Harvard, Vancouver, ISO, and other styles

14

Thakur, Anil, and Anand K. Bachhawat. "The role of transmembrane domain 9 in substrate recognition by the fungal high-affinity glutathione transporters." Biochemical Journal 429, no. 3 (2010): 593–602. http://dx.doi.org/10.1042/bj20100240.

Full text

Abstract:

Hgt1p, a high-affinity glutathione transporter from Saccharomyces cerevisiae belongs to the recently described family of OPTs (oligopeptide transporters), the majority of whose members still have unknown substrate specificity. To obtain insights into substrate recognition and translocation, we have subjected all 21 residues of TMD9 (transmembrane domain 9) to alanine-scanning mutagenesis. Phe523 was found to be critical for glutathione recognition, since F523A mutants showed a 4-fold increase in Km without affecting expression or localization. Phe523 and the previously identified polar residue

APA, Harvard, Vancouver, ISO, and other styles

15

Gray, F., F. Chrétien, A. V. Decouvelaere, et al. "Expression du transporteur de haute affinité du glutamate EAAT-1 par les cellules macrophagiques et microgliales activées dans les maladies à prions." Revue Neurologique 160, no. 8-9 (2004): 846. http://dx.doi.org/10.1016/s0035-3787(04)71045-0.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

Escudero, Leticia, Vicente Mariscal, and Enrique Flores. "Functional Dependence between Septal Protein SepJ from Anabaena sp. Strain PCC 7120 and an Amino Acid ABC-Type Uptake Transporter." Journal of Bacteriology 197, no. 16 (2015): 2721–30. http://dx.doi.org/10.1128/jb.00289-15.

Full text

Abstract:

ABSTRACTIn the diazotrophic filaments of heterocyst-forming cyanobacteria, two different cell types, the CO2-fixing vegetative cells and the N2-fixing heterocysts, exchange nutrients, including some amino acids. In the model organismAnabaenasp. strain PCC 7120, the SepJ protein, composed of periplasmic and integral membrane (permease) sections, is located at the intercellular septa joining adjacent cells in the filament. The unicellular cyanobacteriumSynechococcus elongatusstrain PCC 7942 bears a gene,Synpcc7942_1024(here designateddmeA), encoding a permease homologous to the SepJ permease dom

APA, Harvard, Vancouver, ISO, and other styles

17

Welbourne, Tomas C., and James C. Matthews. "Glutamate transport and renal function." American Journal of Physiology-Renal Physiology 277, no. 4 (1999): F501—F505. http://dx.doi.org/10.1152/ajprenal.1999.277.4.f501.

Full text

Abstract:

Brush border γ-glutamyltransferase-glutaminase activity and the high-affinity glutamate transporter EAAC1 function as a unit in generating and transporting extracellular glutamate into proximal tubules as a signal that modulates intracellular glutamine/glutamate metabolism, paracellular permeability, and urinary acidification. The reported presence of a second glutamate transporter, GLT1, on the antiluminal tubule surface points to specific functional roles for each subtype in physiological and pathophysiological processes.

APA, Harvard, Vancouver, ISO, and other styles

18

Yaster, Myron, Xiaowei Guan, Ronald S. Petralia, Jeffery D. Rothstein, Wei Lu, and Yuan-Xiang Tao. "Effect of Inhibition of Spinal Cord Glutamate Transporters on Inflammatory Pain Induced by Formalin and Complete Freund's Adjuvant." Anesthesiology 114, no. 2 (2011): 412–23. http://dx.doi.org/10.1097/aln.0b013e318205df50.

Full text

Abstract:

Background Spinal cord glutamate transporters clear synaptically released glutamate and maintain normal sensory transmission. However, their ultrastructural localization is unknown. Moreover, whether and how they participate in inflammatory pain has not been carefully studied. Methods Immunogold labeling with electron microscopy was carried out to characterize synaptic and nonsynaptic localization of glutamate transporters in the superficial dorsal horn. Their expression and uptake activity after formalin- and complete Freund's adjuvant (CFA)-induced inflammation were evaluated by Western blot

APA, Harvard, Vancouver, ISO, and other styles

19

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 (2010): 2581–86. http://dx.doi.org/10.1152/jn.00018.2010.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

20

Low, S. Y., P. M. Taylor, H. S. Hundal, C. I. Pogson, and M. J. Rennie. "Transport of l-glutamine and l-glutamate across sinusoidal membranes of rat liver. Effects of starvation, diabetes and corticosteroid treatment." Biochemical Journal 284, no. 2 (1992): 333–40. http://dx.doi.org/10.1042/bj2840333.

Full text

Abstract:

There is increasing evidence that membrane transporters for glutamine and glutamate are involved in control of liver metabolism in health and disease. We therefore investigated the effects of three catabolic states [starvation (60 h), diabetes (4 days after streptozotocin treatment) and corticosteroid (8-day dexamethasone) treatment] associated with altered hepatic amino acid metabolism on the activity of glutamine and glutamate transporters in sinusoidal membrane vesicles from livers of treated rats. In control preparations, L-[14C]glutamine uptake was largely Na(+)-dependent, but L-[14C]glut

APA, Harvard, Vancouver, ISO, and other styles

21

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

22

Vandenberg, Robert J., and Renae M. Ryan. "Mechanisms of Glutamate Transport." Physiological Reviews 93, no. 4 (2013): 1621–57. http://dx.doi.org/10.1152/physrev.00007.2013.

Full text

Abstract:

l-Glutamate is the predominant excitatory neurotransmitter in the mammalian central nervous system and plays important roles in a wide variety of brain functions, but it is also a key player in the pathogenesis of many neurological disorders. The control of glutamate concentrations is critical to the normal functioning of the central nervous system, and in this review we discuss how glutamate transporters regulate glutamate concentrations to maintain dynamic signaling mechanisms between neurons. In 2004, the crystal structure of a prokaryotic homolog of the mammalian glutamate transporter fami

APA, Harvard, Vancouver, ISO, and other styles

23

Helms, Hans CC, Blanca I. Aldana, Simon Groth, et al. "Characterization of the L-glutamate clearance pathways across the blood–brain barrier and the effect of astrocytes in an in vitro blood–brain barrier model." Journal of Cerebral Blood Flow & Metabolism 37, no. 12 (2017): 3744–58. http://dx.doi.org/10.1177/0271678x17690760.

Full text

Abstract:

The aim was to characterize the clearance pathways for L-glutamate from the brain interstitial fluid across the blood–brain barrier using a primary in vitro bovine endothelial/rat astrocyte co-culture. Transporter profiling was performed using uptake studies of radiolabeled L-glutamate with co-application of transporter inhibitors and competing amino acids. Endothelial abluminal L-glutamate uptake was almost abolished by co-application of an EAAT-1 specific inhibitor, whereas luminal uptake was inhibited by L-glutamate and L-aspartate (1 mM). L-glutamate uptake followed Michaelis–Menten-like k

APA, Harvard, Vancouver, ISO, and other styles

24

Almalki, Atiah H., Hashem O. Alsaab, Walaa F. Alsanie, et al. "Potential Benefits of N-Acetylcysteine in Preventing Pregabalin-Induced Seeking-Like Behavior." Healthcare 9, no. 4 (2021): 376. http://dx.doi.org/10.3390/healthcare9040376.

Full text

Abstract:

Substance-use disorder is globally prevalent and responsible for numerous social and medical problems. Pregabalin (Lyrica), typically used to treat diabetic neuropathy, has recently emerged as a drug of abuse. Drug abuse is associated with several neuronal changes, including the downregulation of glutamate transporters such as glutamate transporter 1 and cystine/glutamate antiporter. We investigated the effects of N-acetylcysteine, a glutamate transporter 1 and xCT upregulator, on pregabalin addiction using a conditioned place preference paradigm. Pregabalin (60 mg/kg) was found to induce cond

APA, Harvard, Vancouver, ISO, and other styles

25

Mort, Dominic, Païkan Marcaggi, James Grant, and David Attwell. "Effect of Acute Exposure to Ammonia on Glutamate Transport in Glial Cells Isolated From the Salamander Retina." Journal of Neurophysiology 86, no. 2 (2001): 836–44. http://dx.doi.org/10.1152/jn.2001.86.2.836.

Full text

Abstract:

A rise of brain ammonia level, as occurs in liver failure, initially increases glutamate accumulation in neurons and glial cells. We investigated the effect of acute exposure to ammonia on glutamate transporter currents in whole cell clamped glial cells from the salamander retina. Ammonia potentiated the current evoked by a saturating concentration ofl-glutamate, and decreased the apparent affinity of the transporter for glutamate. The potentiation had a Michaelis-Menten dependence on ammonia concentration, with a K m of 1.4 mM and a maximum potentiation of 31%. Ammonia also potentiated the tr

APA, Harvard, Vancouver, ISO, and other styles

26

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 (1999): 604–15. http://dx.doi.org/10.1097/00004647-199906000-00003.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

27

Diamond, Jeffrey S., and Craig E. Jahr. "Synaptically Released Glutamate Does Not Overwhelm Transporters on Hippocampal Astrocytes During High-Frequency Stimulation." Journal of Neurophysiology 83, no. 5 (2000): 2835–43. http://dx.doi.org/10.1152/jn.2000.83.5.2835.

Full text

Abstract:

In addition to maintaining the extracellular glutamate concentration at low ambient levels, high-affinity glutamate transporters play a direct role in synaptic transmission by speeding the clearance of glutamate from the synaptic cleft and limiting the extent to which transmitter spills over between synapses. Transporters are expressed in both neurons and glia, but glial transporters are likely to play the major role in removing synaptically released glutamate from the extracellular space. The role of transporters in synaptic transmission has been studied directly by measuring synaptically act

APA, Harvard, Vancouver, ISO, and other styles

28

Bai, Liqun, Xiaohong Zhang та Fayez K. Ghishan. "Characterization of vesicular glutamate transporter in pancreatic α- and β-cells and its regulation by glucose". American Journal of Physiology-Gastrointestinal and Liver Physiology 284, № 5 (2003): G808—G814. http://dx.doi.org/10.1152/ajpgi.00333.2002.

Full text

Abstract:

Glutamate has been suggested to play an important role in the release of insulin and glucagon from pancreatic cells via exocytosis. Vesicular glutamate transporter is a rate-limiting step for glutamate release and is involved in the glutamate-evoked exocytosis. Two vesicular glutamate transporters (VGLUT1 and -2) have recently been cloned from the brain. In this report, we first functionally characterized vesicular glutamate transporter in cultured pancreatic α- and β-cells, and then detected mRNA expression of VGLUT1 and -2 in these cells. We also investigated the effect of high or low level

APA, Harvard, Vancouver, ISO, and other styles

29

Wang, Jiali, Peifan Li, Xiaozhen Yu, and Christof Grewer. "Observing spontaneous, accelerated substrate binding in molecular dynamics simulations of glutamate transporters." PLOS ONE 16, no. 4 (2021): e0250635. http://dx.doi.org/10.1371/journal.pone.0250635.

Full text

Abstract:

Glutamate transporters are essential for removing the neurotransmitter glutamate from the synaptic cleft. Glutamate transport across the membrane is associated with elevator-like structural changes of the transport domain. These structural changes require initial binding of the organic substrate to the transporter. Studying the binding pathway of ligands to their protein binding sites using molecular dynamics (MD) simulations requires micro-second level simulation times. Here, we used three methods to accelerate aspartate binding to the glutamate transporter homologue Gltph and to investigate

APA, Harvard, Vancouver, ISO, and other styles

30

Carter, P., and T. Welbourne. "Glutamate transport regulation of renal glutaminase flux in vivo." American Journal of Physiology-Endocrinology and Metabolism 273, no. 3 (1997): E521. http://dx.doi.org/10.1152/ajpendo.1997.273.3.e521.

Full text

Abstract:

We proposed that glutamate transport into cultured kidney cells represses cellular glutaminase activity and hence regulates glutamine utilization. To test this putative regulatory mechanism in vivo, glutamine uptake and conversion to glutamate as well as ammonium production were measured in the intact functioning rat kidney. Glutamine uptake was determined as net removal, arteriovenous concentration difference times renal plasma flow, and also as unidirectional uptake from the fractional extraction of tracer L-[14C]glutamine. Ammonium production was measured as that released into the renal vei

APA, Harvard, Vancouver, ISO, and other styles

31

Hu, Qiu Xiang, Sigrid Ottestad-Hansen, Silvia Holmseth, Bjørnar Hassel, Niels Christian Danbolt, and Yun Zhou. "Expression of Glutamate Transporters in Mouse Liver, Kidney, and Intestine." Journal of Histochemistry & Cytochemistry 66, no. 3 (2018): 189–202. http://dx.doi.org/10.1369/0022155417749828.

Full text

Abstract:

Glutamate transport activities have been identified not only in the brain, but also in the liver, kidney, and intestine. Although glutamate transporter distributions in the central nervous system are fairly well known, there are still uncertainties with respect to the distribution of these transporters in peripheral organs. Quantitative information is mostly lacking, and few of the studies have included genetically modified animals as specificity controls. The present study provides validated qualitative and semi-quantitative data on the excitatory amino acid transporter (EAAT)1–3 subtypes in

APA, Harvard, Vancouver, ISO, and other styles

32

WINKLER, BARRY S., NATALIA KAPOUSTA-BRUNEAU, MATTHEW J. ARNOLD, and DANIEL G. GREEN. "Effects of inhibiting glutamine synthetase and blocking glutamate uptake on b-wave generation in the isolated rat retina." Visual Neuroscience 16, no. 2 (1999): 345–53. http://dx.doi.org/10.1017/s095252389916214x.

Full text

Abstract:

The purpose of the present experiments was to evaluate the contribution of the glutamate-glutamine cycle in retinal glial (Müller) cells to photoreceptor cell synaptic transmission. Dark-adapted isolated rat retinas were superfused with oxygenated bicarbonate-buffered media. Recordings were made of the b-wave of the electroretinogram as a measure of light-induced photoreceptor to ON-bipolar neuron transmission. L-methionine sulfoximine (1–10 mM) was added to superfusion media to inhibit glutamine synthetase, a Müller cell specific enzyme, by more than 99% within 5–10 min, thereby disrupting th

APA, Harvard, Vancouver, ISO, and other styles

33

Lee, Wha-Joon, Richard A. Hawkins, Juan R. Viña, and Darryl R. Peterson. "Glutamine transport by the blood-brain barrier: a possible mechanism for nitrogen removal." American Journal of Physiology-Cell Physiology 274, no. 4 (1998): C1101—C1107. http://dx.doi.org/10.1152/ajpcell.1998.274.4.c1101.

Full text

Abstract:

Glutamine and glutamate transport activities were measured in isolated luminal and abluminal plasma membrane vesicles derived from bovine brain endothelial cells. Facilitative systems for glutamine and glutamate were almost exclusively located in luminal-enriched membranes. The facilitative glutamine carrier was neither sensitive to 2-aminobicyclo(2,2,1)heptane-2-carboxylic acid inhibition nor did it participate in accelerated amino acid exchange; it therefore appeared to be distinct from the neutral amino acid transport system L1. Two Na-dependent glutamine transporters were found in ablumina

APA, Harvard, Vancouver, ISO, and other styles

34

Ji, Yurui, Vincent L. G. Postis, Yingying Wang, Mark Bartlam, and Adrian Goldman. "Transport mechanism of a glutamate transporter homologue GltPh." Biochemical Society Transactions 44, no. 3 (2016): 898–904. http://dx.doi.org/10.1042/bst20160055.

Full text

Abstract:

Glutamate transporters are responsible for uptake of the neurotransmitter glutamate in mammalian central nervous systems. Their archaeal homologue GltPh, an aspartate transporter isolated from Pyrococcus horikoshii, has been the focus of extensive studies through crystallography, MD simulations and single-molecule FRET (smFRET). Here, we summarize the recent research progress on GltPh, in the hope of gaining some insights into the transport mechanism of this aspartate transporter.

APA, Harvard, Vancouver, ISO, and other styles

35

Kanner, B. I., M. P. Kavanaugh, and A. Bendahan. "Molecular characterization of substrate-binding sites in the glutamate transporter family." Biochemical Society Transactions 29, no. 6 (2001): 707–10. http://dx.doi.org/10.1042/bst0290707.

Full text

Abstract:

Glutamate transporters are essential for terminating synaptic excitation and for maintaining extracellular glutamate concentrations below neurotoxic levels. These transporters also mediate a thermodynamically uncoupled chloride flux that is activated by two of the molecules that they transport – sodium and glutamate. Five eukaryotic glutamate transporters have been cloned and identified. They exhibit ~ 50% identity and this homology is even greater in the carboxyl terminal half, which is predicted to have an unusual topology. Determination of the topology shows that the carboxyl terminal part

APA, Harvard, Vancouver, ISO, and other styles

36

Tamarappoo, B. K., M. Nam, M. S. Kilberg, and T. C. Welbourne. "Glucocorticoid regulation of splanchnic glutamine, alanine, glutamate, ammonia, and glutathione fluxes." American Journal of Physiology-Endocrinology and Metabolism 264, no. 4 (1993): E526—E533. http://dx.doi.org/10.1152/ajpendo.1993.264.4.e526.

Full text

Abstract:

Interorgan glutamine and associated metabolite fluxes were measured across the gut and liver to delineate splanchnic bed fluxes secondary to enhanced arterial loads mobilized in the periphery by glucocorticoid. Experiments were performed on adrenalectomized rats since adrenalectomy doubled the hepatic glucocorticoid receptor population compared with intact animals. Under these conditions, triamcinolone supplement (40 micrograms.day-1.100 g body wt-1) enhanced the combined net glutamine uptake by gut and liver eightfold, whereas combined gut and liver unidirectional breakdown and synthesis flux

APA, Harvard, Vancouver, ISO, and other styles

37

Holley, David C., and Michael P. Kavanaugh. "Interactions of alkali cations with glutamate transporters." Philosophical Transactions of the Royal Society B: Biological Sciences 364, no. 1514 (2008): 155–61. http://dx.doi.org/10.1098/rstb.2008.0246.

Full text

Abstract:

The transport of glutamate is coupled to the co-transport of three Na + ions and the countertransport of one K + ion. In addition to this carrier-type exchange behaviour, glutamate transporters also behave as chloride channels. The chloride channel activity is strongly influenced by the cations that are involved in coupled flux, making glutamate transporters representative of the ambiguous interface between carriers and channels. In this paper, we review the interaction of alkali cations with glutamate transporters in terms of these diverse functions. We also present a model derived from elect

APA, Harvard, Vancouver, ISO, and other styles

38

DAVIS, R. E. "Action of excitatory amino acids on hypodermis and the motornervous system of Ascaris suum: pharmacological evidence for a glutamate transporter." Parasitology 116, no. 5 (1998): 487–500. http://dx.doi.org/10.1017/s0031182098002479.

Full text

Abstract:

Electrophysiological and pharmacological experiments suggest the presence of an electrogenic glutamate transporter in the motornervous system of the parasitic nematode Ascaris suum. This putative transporter occurs in hypodermis (a tissue in some respects analogous to glia) and in DE2 motorneurons, a dorsal excitatory motorneuron class which receives excitatory glutamatergic post-synaptic potentials. Glutamate application to hypodermis produced non-conductance mediated depolarizations that were smaller in amplitude and slower in rate of rise than DE2 responses where a glutamate-activated condu

APA, Harvard, Vancouver, ISO, and other styles

39

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 (2004): 551–65. http://dx.doi.org/10.1017/s0952523804214067.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

40

Low, S. Y., P. M. Taylor, A. Ahmed, C. I. Pogson, and M. J. Rennie. "Substrate-specificity of glutamine transporters in membrane vesicles from rat liver and skeletal muscle investigated using amino acid analogues." Biochemical Journal 278, no. 1 (1991): 105–11. http://dx.doi.org/10.1042/bj2780105.

Full text

Abstract:

We investigated the effects of glutamine and histidine analogues on glutamine transport processes in membrane vesicles prepared from rat liver (sinusoidal membrane) and skeletal muscle (sarcolemma). L-[14C]Glutamine is transported in these membranes predominantly by Systems N/Nm (liver and muscle respectively), and to a lesser extent by Systems A and L (e.g. about 60, 20 and 20% of total flux respectively via Systems N, A and L at 0.05 mM-glutamine in liver membrane vesicles). The glutamine anti-metabolites 6-diazo-5-oxo-L-norleucine and acivicin were relatively poor inhibitors of glutamine up

APA, Harvard, Vancouver, ISO, and other styles

41

Grant, George B., and Frank S. Werblin. "A glutamate-elicited chloride current with transporter-like properties in rod photoreceptors of the tiger salamander." Visual Neuroscience 13, no. 1 (1996): 135–44. http://dx.doi.org/10.1017/s0952523800007185.

Full text

Abstract:

AbstractGlutamate, when puffed near the synaptic terminals, elicits a current in rod photoreceptors. The current is strongly dependent upon both the intracellular and extracellular chloride concentration: its reversal potential follows the predicted Nernst potential for a chloride permeable channel. The glutamate-elicited current also requires the presence of extracellular sodium. This glutamate-elicited current is pharmacologically like a glutamate transporter: it is elicited, in order of efficacy, by L-glutamate, L-aspartate, L-cysteate, D-aspartate, and D-glutamate, all shown to activate gl

APA, Harvard, Vancouver, ISO, and other styles

42

Rimaniol, Anne-Cécile, Patricia Mialocq, Pascal Clayette, Dominique Dormont, and Gabriel Gras. "Role of glutamate transporters in the regulation of glutathione levels in human macrophages." American Journal of Physiology-Cell Physiology 281, no. 6 (2001): C1964—C1970. http://dx.doi.org/10.1152/ajpcell.2001.281.6.c1964.

Full text

Abstract:

Cysteine is the limiting precursor for glutathione synthesis. Because of its low bioavailability, cysteine is generally produced from cystine, which may be taken up through two different transporters. The cystine/glutamate antiporter (x[Formula: see text] system) transports extracellular cystine in exchange for intracellular glutamate. The XAG transport system takes up extracellular cystine, glutamate, and aspartate. Both are sensitive to competition between cystine and glutamate, and excess extracellular glutamate thus inhibits glutathione synthesis, a nonexcitotoxic mechanism for glutamate t

APA, Harvard, Vancouver, ISO, and other styles

43

Kinney, Gregory A., and William J. Spain. "Synaptically Evoked GABA Transporter Currents in Neocortical Glia." Journal of Neurophysiology 88, no. 6 (2002): 2899–908. http://dx.doi.org/10.1152/jn.00037.2002.

Full text

Abstract:

The presence, magnitude, and time course of GABA transporter currents were investigated in electrophysiologically characterized neocortical astrocytes in an in vitro slice preparation. On stimulation with a bipolar-tungsten stimulating electrode placed nearby, the majority of cells tested displayed long-lasting GABA transporter currents using both single and repetitive stimulation protocols. Using subtype-specific GABA transporter antagonists, long-lasting GABA transporter currents were identified in neocortical astrocytes that originated from at least two subtypes of GABA transporters: GAT-1

APA, Harvard, Vancouver, ISO, and other styles

44

Slotboom, Dirk Jan, Wil N. Konings, and Juke S. Lolkema. "Glutamate transporters combine transporter- and channel-like features." Trends in Biochemical Sciences 26, no. 9 (2001): 534–39. http://dx.doi.org/10.1016/s0968-0004(01)01925-9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

45

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 (2018): 106–25. http://dx.doi.org/10.3390/neuroglia1010009.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

46

Qureshi, Tayyaba, Mona Bjørkmo, Kaja Nordengen, et al. "Slc38a1 Conveys Astroglia-Derived Glutamine into GABAergic Interneurons for Neurotransmitter GABA Synthesis." Cells 9, no. 7 (2020): 1686. http://dx.doi.org/10.3390/cells9071686.

Full text

Abstract:

GABA signaling is involved in a wide range of neuronal functions, such as synchronization of action potential firing, synaptic plasticity and neuronal development. Sustained GABA signaling requires efficient mechanisms for the replenishment of the neurotransmitter pool of GABA. The prevailing theory is that exocytotically released GABA may be transported into perisynaptic astroglia and converted to glutamine, which is then shuttled back to the neurons for resynthesis of GABA—i.e., the glutamate/GABA-glutamine (GGG) cycle. However, an unequivocal demonstration of astroglia-to-nerve terminal tra

APA, Harvard, Vancouver, ISO, and other styles

47

Do, Sang-Hwan, Ganesan L. Kamatchi, Jacqueline M. Washington, and Zhiyi Zuo. "Effects of Volatile Anesthetics on Glutamate Transporter, Excitatory Amino Acid Transporter Type 3." Anesthesiology 96, no. 6 (2002): 1492–97. http://dx.doi.org/10.1097/00000542-200206000-00032.

Full text

Abstract:

Background Glutamate transporters play an important role in maintaining extracellular glutamate homeostasis. The authors studied the effects of volatile anesthetics on one type of glutamate transporters, excitatory amino acid transporter type 3 (EAAT3), and the role of protein kinase C in mediating these effects. Methods Excitatory amino acid transporter type 3 was expressed in Xenopus oocytes by injection of EAAT3 mRNA. Using two-electrode voltage clamp, membrane currents were recorded before, during, and after application of L-glutamate. Responses were quantified by integrating the current t

APA, Harvard, Vancouver, ISO, and other styles

48

Gandasi, Nikhil R., Vasiliki Arapi, Michel E. Mickael, et al. "Glutamine Uptake via SNAT6 and Caveolin Regulates Glutamine–Glutamate Cycle." International Journal of Molecular Sciences 22, no. 3 (2021): 1167. http://dx.doi.org/10.3390/ijms22031167.

Full text

Abstract:

SLC38A6 (SNAT6) is the only known member of the SLC38 family that is expressed exclusively in the excitatory neurons of the brain. It has been described as an orphan transporter with an unknown substrate profile, therefore very little is known about SNAT6. In this study, we addressed the substrate specificity, mechanisms for internalization of SNAT6, and the regulatory role of SNAT6 with specific insights into the glutamate–glutamine cycle. We used tritium-labeled amino acids in order to demonstrate that SNAT6 is functioning as a glutamine and glutamate transporter. SNAT6 revealed seven predic

APA, Harvard, Vancouver, ISO, and other styles

49

Muscoli, Carolina, Concetta Dagostino, Sara Ilari, et al. "Posttranslational Nitration of Tyrosine Residues Modulates Glutamate Transmission and Contributes to N-Methyl-D-aspartate-Mediated Thermal Hyperalgesia." Mediators of Inflammation 2013 (2013): 1–12. http://dx.doi.org/10.1155/2013/950947.

Full text

Abstract:

Activation of the N-methyl-D-aspartate receptor (NMDAR) is fundamental in the development of hyperalgesia. Overactivation of this receptor releases superoxide and nitric oxide that, in turn, forms peroxynitrite (PN). All of these events have been linked to neurotoxicity. The receptors and enzymes involved in the handling of glutamate pathway—specifically NMDARs, glutamate transporter, and glutamine synthase (GS)—have key tyrosine residues which are targets of the nitration process causing subsequent function modification. Our results demonstrate that the thermal hyperalgesia induced by intrath

APA, Harvard, Vancouver, ISO, and other styles

50

Picaud, S. A., H. P. Larsson, G. B. Grant, H. Lecar, and F. S. Werblin. "Glutamate-gated chloride channel with glutamate-transporter-like properties in cone photoreceptors of the tiger salamander." Journal of Neurophysiology 74, no. 4 (1995): 1760–71. http://dx.doi.org/10.1152/jn.1995.74.4.1760.

Full text

Abstract:

1. Using the patch-clamp technique, we investigated whether the glutamate-elicited current in mechanically isolated cone photoreceptors from the salamander retina is generated by a Cl- channel or a glutamate transporter. 2. The current reversed near the equilibrium potential for Cl-, was decreased by three Cl- channel blockers, 5-nitro-2-(3-phenyl-propylamino) benzoic acid, 4,4'-diisothiocyanostilbene-2,2'-disulfonate, and diphenylamine 2,2'-dicarboxylic acid, and was eliminated when gluconate was substituted for both internal and external Cl-, features consistent with the current being mediat

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!