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Journal articles on the topic 'Sodium-dependent glutamate/aspartate transporter 1'

Author: Grafiati

Published: 4 June 2025

Last updated: 1 August 2025

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1

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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2

Guskov, Albert, Sonja Jensen, Stephan Rempel, Inga Hänelt, and Dirk Slotboom. "Elevator mechanism of aspartate (glutamate) transport across the membrane." Acta Crystallographica Section A Foundations and Advances 70, a1 (2014): C1491. http://dx.doi.org/10.1107/s2053273314085088.

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Archaeal homologues of human neuronal glutamate transporter catalyze the coupled uptake of aspartate and three sodium ions. After the delivery of the substrate and sodium ions in the cytoplasm the empty binding site must reorient to the outward-facing conformation to reset the transporter. Here we present a crystal structure of the substrate-free transporter GltTk from Thermococcus kodakarensis, resolved at 3 Å resolution [1]. Despite the global similarity to the previously resolved structures of aspartate transporter GltPh, there are tremendous rearrangements in the substrate-binding site. Th

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3

Burckhardt, Birgitta C., and Gerhard Burckhardt. "Interaction of Excitatory Amino Acid Transporters 1 – 3 (EAAT1, EAAT2, EAAT3) with N-Carbamoylglutamate and N-Acetylglutamate." Cellular Physiology and Biochemistry 43, no. 5 (2017): 1907–16. http://dx.doi.org/10.1159/000484110.

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Background/Aims: Inborn deficiency of the N-acetylglutamate synthase (NAGS) impairs the urea cycle and causes neurotoxic hyperammonemia. Oral administration of N-carbamoylglutamate (NCG), a synthetic analog of N-acetylglutamate (NAG), successfully decreases plasma ammonia levels in the affected children. Due to structural similarities to glutamate, NCG may be absorbed in the intestine and taken up into the liver by excitatory amino acid transporters (EAATs). Methods: Using Xenopus laevis oocytes expressing either human EAAT1, 2, or 3, or human sodium-dependent dicarboxylate transporter 3 (NaDC

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4

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.

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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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5

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.

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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

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6

Takarada, T., E. Hinoi, VJ Balcar, H. Taniura, and Y. Yoneda. "Possible expression of functional glutamate transporters in the rat testis." Journal of Endocrinology 181, no. 2 (2004): 233–44. http://dx.doi.org/10.1677/joe.0.1810233.

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Neither expression nor functionality is clear in peripheral tissues with the molecular machineries required for excitatory neurotransmitter signaling by L-glutamate (Glu) in the central nervous system, while a recent study has shown that several Glu receptors are functionally expressed in the rat testis. This fact prompted us to explore the possible functional expression in the rat testis of the Glu transporters usually responsible for the regulation of extracellular Glu concentrations in the brain. RT-PCR revealed the expression, in the rat testis, of mRNA for five different subtypes of Glu t

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7

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 (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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8

Mordrelle, Agnès, Eric Jullian, Cyrille Costa, et al. "EAAT1 is involved in transport ofl-glutamate during differentiation of the Caco-2 cell line." American Journal of Physiology-Gastrointestinal and Liver Physiology 279, no. 2 (2000): G366—G373. http://dx.doi.org/10.1152/ajpgi.2000.279.2.g366.

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Little is known concerning the expression of amino acid transporters during intestinal epithelial cell differentiation. The transport mechanism ofl-glutamate and its regulation during the differentiation process were investigated using the human intestinal Caco-2 cell line. Kinetic studies demonstrated the presence of a single, high-affinity,d-aspartate-sensitive l-glutamate transport system in both confluent and fully differentiated Caco-2 cells. This transport was clearly Na+ dependent, with a Hill coefficient of 2.9 ± 0.3, suggesting a 3 Na+-to-1 glutamate stoichiometry and corresponding to

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9

Wingrove, T. G., and G. A. Kimmich. "Low-affinity intestinal L-aspartate transport with 2:1 coupling stoichiometry for Na+/Asp." American Journal of Physiology-Cell Physiology 255, no. 6 (1988): C737—C744. http://dx.doi.org/10.1152/ajpcell.1988.255.6.c737.

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Epithelial cells isolated from chick small intestine were used to define the ionic and electrical characteristics of a low-affinity (Km = 4.1 mM) L-aspartate transport system. L-Glutamate and D-aspartate, but not D-glutamate, were found to inhibit L-aspartate influx, suggesting that this uptake system has a substrate specificity similar to that previously described for a high-affinity (Km = 16 microM) acidic amino acid transporter in the same cells. Low-affinity uptake is Na+ dependent with a Hill coefficient (n) of 1.4. Intracellular K+ moderately enhances but is not required for aspartate in

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10

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.

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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

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Chiu, Martina, Erika Griffini, Denise Toscani, et al. "Glutamine Addiction of Multiple Myeloma Cells Reprograms Mesenchymal Stromal Cell Enzymes and Transporters Towards a Pro-Tumor Phenotype." Blood 142, Supplement 1 (2023): 4680. http://dx.doi.org/10.1182/blood-2023-186637.

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Metabolic alterations in cancer are not only functional to ensure malignant cell growth but also shape a pro-tumor behavior of normal cell populations in the tumor microenvironment. Multiple myeloma (MM) is the only human cancer that is both glutamine-addicted and glutamine-auxotroph, a feature that renders MM growth completely dependent upon extracellular glutamine availability. Indeed, plasma cells from most MM patients do not express Glutamine Synthetase (GS), the only enzyme able to synthetize glutamine from glutamate and ammonium, while express high levels of Glutaminase (GLS), which cata

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12

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 (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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13

MARKERT, JAMES M., CATHERINE M. FULLER, G. YANCEY GILLESPIE, et al. "Differential gene expression profiling in human brain tumors." Physiological Genomics 5, no. 1 (2001): 21–33. http://dx.doi.org/10.1152/physiolgenomics.2001.5.1.21.

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Gene expression profiling of three human temporal lobe brain tissue samples (normal) and four primary glioblastoma multiforme (GBM) tumors using oligonucleotide microarrays was done. Moreover, confirmation of altered expression was performed by whole cell patch clamp, immunohistochemical staining, and RT-PCR. Our results identified several ion and solute transport-related genes, such as N-methyl-d-aspartate (NMDA) receptors, α-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA)-2 receptors, GABAA receptor subunits α3, β1, β2, and β3, the glutamate transporter, the glutamate/aspartate transp

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14

Plakidou-Dymock, S., and J. D. McGivan. "Regulation of the glutamate transporter by amino acid deprivation and associated effects on the level of EAAC1 mRNA in the renal epithelial cell line NBL-I." Biochemical Journal 295, no. 3 (1993): 749–55. http://dx.doi.org/10.1042/bj2950749.

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The glutamate transport system of the bovine renal epithelial cell line NBL-1 was studied. The Km for Na(+)-dependent glutamate transport was found to be 13.8 +/- 2.4 microM (Vmax. 365 +/- 19.2 pmol/3 min per mg) and for Na(+)-dependent aspartate transport 4.5 +/- 1.1 microM (Vmax. 108 +/- 6.3 pmol/3 min per mg). The Km values are in close agreement with those expected for high-affinity Na(+)-dependent glutamate transport by System XAG-. Upon deprivation of amino acids, the Vmax. for Na+/aspartate co-transport rose to 203 +/- 6.0 pmol/3 min per mg (Km 3.8 +/- 0.5 microns). A probe was construc

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15

Nishimura, Mitsuhiro, Kohji Sato, Tomoya Okada, et al. "Ketamine Inhibits Monoamine Transporters Expressed in Human Embryonic Kidney 293 Cells." Anesthesiology 88, no. 3 (1998): 768–74. http://dx.doi.org/10.1097/00000542-199803000-00029.

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Background Ketamine has been characterized as having psychotomimetic and sympathomimetic effects. These symptoms have raised the possibility that ketamine affects monoaminergic neurotransmission. To elucidate the relation between ketamine and monoamine transporters, the authors constructed three cell lines that stably express the norepinephrine, dopamine, and serotonin transporters and investigated the effects of ketamine on these transporters. Methods Human embryonic kidney cells were transfected using the Chen-Okayama method with the human norepinephrine, rat dopamine, and rat serotonin tran

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16

Napier, Ian A., Sarasa A. Mohammadi, and MacDonald J. Christie. "Glutamate transporter dysfunction associated with nerve injury-induced pain in mice." Journal of Neurophysiology 107, no. 2 (2012): 649–57. http://dx.doi.org/10.1152/jn.00763.2011.

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Dysfunction at glutamatergic synapses has been proposed as a mechanism in the development of neuropathic pain. Here we sought to determine whether peripheral nerve injury-induced neuropathic pain results in functional changes to primary afferent synapses. Signs of neuropathic pain as well as an induction of glial fibrillary acidic protein in immunostained spinal cord sections 4 days after partial ligation of the sciatic nerve indicated the induction of neuropathic pain. We found that following nerve injury, no discernable change to kinetics of dl-α-amino-3-hydroxy-5-methylisoxazole-propionic a

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17

Koochaki, Pooneh, Jesse A. Coker, Biao Qiu, et al. "Abstract 6911: Investigating pharmacological targeting of the SLC1A1 aspartate/glutamate transporter." Cancer Research 85, no. 8_Supplement_1 (2025): 6911. https://doi.org/10.1158/1538-7445.am2025-6911.

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Abstract Background: SLC1A1/EAAT3 functions as a trimeric, Na+-dependent dicarboxylic amino acids (glutamate and aspartate) transporter. Recent studies have identified SLC1A1/EAAT3 as an oncogenic dependency in several cancers, including clear cell renal cell carcinoma (ccRCC), blood-borne tumors, and lung cancer. Unfortunately, despite this transporter’s potential as a therapeutic target, pharmacological inhibition of SLC1A1 has remained elusive due to the absence of potent and selective inhibitors. In earlier studies, we investigated a previously described bicyclic imidazopyridine aniline SL

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18

Waxman, Elisa A., Isabelle Baconguis, David R. Lynch, and Michael B. Robinson. "N-Methyl-d-aspartate Receptor-dependent Regulation of the Glutamate Transporter Excitatory Amino Acid Carrier 1." Journal of Biological Chemistry 282, no. 24 (2007): 17594–607. http://dx.doi.org/10.1074/jbc.m702278200.

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19

Zabłocka, Barbara, and Krystyna Domańska-Janik. "Enhancement of [3H]D-aspartate release during ischemia like conditions in rat hippocampal slices: source of excitatory amino acids." Acta Neurobiologiae Experimentalis 56, no. 1 (1996): 63–70. http://dx.doi.org/10.55782/ane-1996-1105.

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Ischemic neuronal injury is supposed to be caused in part by the extracellular accumulation of excitatory amino acids (EAA). Neurotransmitter and metabolic EAA can be released from synaptic vesicles and cytoplasm of neurones and glial cells. In this study the release of the glutamate analogue [3H]D-aspartate ([3H]D-ASP), loaded into 500-micrometer slices of rat hippocampus, was investigated. The efflux of the label was measured during anoxic - aglycemic ("ischemic") and normoxic K+ depolarization. To identify the pools from which [3H]D-ASP is released we have estimated its calcium dependence a

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20

Lu, Cheng-Wei, Tzu-Yu Lin, Kuan-Ming Chiu, Ming-Yi Lee, and Su-Jane Wang. "Gypenoside XVII Reduces Synaptic Glutamate Release and Protects against Excitotoxic Injury in Rats." Biomolecules 14, no. 5 (2024): 589. http://dx.doi.org/10.3390/biom14050589.

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Excitotoxicity is a common pathological process in neurological diseases caused by excess glutamate. The purpose of this study was to evaluate the effect of gypenoside XVII (GP-17), a gypenoside monomer, on the glutamatergic system. In vitro, in rat cortical nerve terminals (synaptosomes), GP-17 dose-dependently decreased glutamate release with an IC50 value of 16 μM. The removal of extracellular Ca2+ or blockade of N-and P/Q-type Ca2+ channels and protein kinase A (PKA) abolished the inhibitory effect of GP-17 on glutamate release from cortical synaptosomes. GP-17 also significantly reduced t

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21

Reichelt, W., and T. Knöpfel. "Glutamate Uptake Controls Expression of a Slow Postsynaptic Current Mediated by mGluRs in Cerebellar Purkinje Cells." Journal of Neurophysiology 87, no. 4 (2002): 1974–80. http://dx.doi.org/10.1152/jn.00704.2001.

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At the cerebellar parallel fiber-Purkinje cell synapse, isolated presynaptic activity induces fast excitatory postsynaptic currents via ionotropic glutamate receptors while repetitive, high-frequency, presynaptic activity can also induce a slow excitatory postsynaptic current that is mediated by metabotropic glutamate receptors (mGluR1-EPSC). Here we investigated the involvement of glutamate uptake in the expression of the mGluR1-EPSC. Inhibitors of glutamate uptake led to a large increase of the mGluR1-EPSC. d-aspartate (0.4 mM) andl(−)-threo-3-hydroxyaspartate (0.4 mM) increased the mGluR1-E

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22

Velaz-Faircloth, M., T. S. McGraw, M. S. alandro, R. T. Fremeau, M. S. Kilberg, and K. J. Anderson. "Characterization and distribution of the neuronal glutamate transporter EAAC1 in rat brain." American Journal of Physiology-Cell Physiology 270, no. 1 (1996): C67—C75. http://dx.doi.org/10.1152/ajpcell.1996.270.1.c67.

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The extracellular concentration of glutamate and other related excitatory amino acids (EAA) is regulated by the action of transporter proteins located on either presynaptic terminals or adjacent astroglial processes. Recent molecular advances have led to the cloning of three separate cDNAs encoding for Na(+)-dependent glutamate transporters; two are thought to be primarily glial in origin (GLAST and GLT-1) and the third (EAAC1) is localized to neurons in the brain and other nonneural tissues. An EAAC1 cDNA was initially cloned from rabbit small intestine (13). In this study, we report isolatio

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23

Zaleska, Margaret M., Cathleen Gonzales, Sina Djali, and Lee A. Dawson. "GLIAL GLUTAMATE TRANSPORTER GLT-1 DOES NOT REVERSE ITS FUNCTION IN ISCHEMIC PENUMBRA." Stroke 32, suppl_1 (2001): 316. http://dx.doi.org/10.1161/str.32.suppl_1.316-c.

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4 Functional glutamate uptake systems are critical for maintenance of normal synaptic transmission. Several studies have shown that in severely ischemic brain regions, massive efflux of excitatory amino acids (EAAs) results, in large portion, from the reversal of Na + -dependent glutamate transporters. This study was designed to examine the function of the predominant glial transporter, GLT-1, in a brain area representative of ischemic penumbra. Spontaneously hypertensive rats were subjected to a 45 min transient focal ischemia by intraluminal occlusion of the middle cerebral artery (MCAO). In

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24

Kataoka, Y., and H. Ohmori. "Of known neurotransmitters, glutamate is the most likely to be released from chick cochlear hair cells." Journal of Neurophysiology 76, no. 3 (1996): 1870–79. http://dx.doi.org/10.1152/jn.1996.76.3.1870.

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1. Experiments were performed to identify the excitatory amino acid (EAA) released from cochlear hair cells isolated from chick. An isolated hair cell was transported and closely apposed to a cultured granule cell or a Purkinje cell, and current responses were studied in these cell pairs when the apposed hair cell was depolarized. 2. The apposed hair cell was voltage clamped at -65 mV by a nystatin perforated-patch recording technique and the membrane potential was step changed to -10 or 0 mV to induce a release of neurotransmitter. In the granule cell voltage clamped at +55 mV, the hair cell

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Burckhardt, Birgitta C., Julia Lorenz, Christoph Kobbe, and Gerhard Burckhardt. "Substrate specificity of the human renal sodium dicarboxylate cotransporter, hNaDC-3, under voltage-clamp conditions." American Journal of Physiology-Renal Physiology 288, no. 4 (2005): F792—F799. http://dx.doi.org/10.1152/ajprenal.00360.2004.

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Proximal tubule cells extract dicarboxylates from filtrate and blood, using cotransporters located in the brush border [sodium dicarboxylate cotransporter (NaDC-1)] and basolateral cell membrane (NaDC-3). We expressed the human NaDC-3 (hNaDC-3) in Xenopus laevis oocytes and characterized it by the two-electrode voltage-clamp technique. At −60 mV, succinate (4 carbons) and glutarate (5 carbons) generated inward currents due to translocation of three sodium ions and one divalent dicarboxylate, whereas oxalate (2 carbons) and malonate (3 carbons) did not. The cis-dicarboxylate maleate produced cu

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Ramírez-Sotelo, Guadalupe, Esther López-Bayghen, L. Clara R. Hernández-Kelly, J. Antonio Arias-Montaño, Alfonso Bernabé, and Arturo Ortega. "Regulation of the Mouse Na+-Dependent Glutamate/Aspartate Transporter GLAST: Putative Role of an AP-1 DNA Binding Site." Neurochemical Research 32, no. 1 (2006): 73–80. http://dx.doi.org/10.1007/s11064-006-9227-3.

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27

Bicket, Alex, Pedram Mehrabi, Zlatina Naydenova, et al. "Novel regulation of equlibrative nucleoside transporter 1 (ENT1) by receptor-stimulated Ca2+-dependent calmodulin binding." American Journal of Physiology-Cell Physiology 310, no. 10 (2016): C808—C820. http://dx.doi.org/10.1152/ajpcell.00243.2015.

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Equilibrative nucleoside transporters (ENTs) facilitate the flux of nucleosides, such as adenosine, and nucleoside analog (NA) drugs across cell membranes. A correlation between adenosine flux and calcium-dependent signaling has been previously reported; however, the mechanistic basis of these observations is not known. Here we report the identification of the calcium signaling transducer calmodulin (CaM) as an ENT1-interacting protein, via a conserved classic 1-5-10 motif in ENT1. Calcium-dependent human ENT1-CaM protein interactions were confirmed in human cell lines (HEK293, RT4, U-87 MG) u

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Postnikova, Tatyana Y., Sergey L. Malkin, Maria V. Zakharova, Ilya V. Smolensky, Olga E. Zubareva, and Aleksey V. Zaitsev. "Ceftriaxone Treatment Weakens Long-Term Synaptic Potentiation in the Hippocampus of Young Rats." International Journal of Molecular Sciences 22, no. 16 (2021): 8417. http://dx.doi.org/10.3390/ijms22168417.

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Disrupted glutamate clearance in the synaptic cleft leads to synaptic dysfunction and neurological diseases. Decreased glutamate removal from the synaptic cleft is known to cause excitotoxicity. Data on the physiological effects of increased glutamate clearance are contradictory. This study investigated the consequences of ceftriaxone (CTX), an enhancer of glutamate transporter 1 expression, treatment on long-term synaptic potentiation (LTP) in the hippocampus of young rats. In this study, 5-day administration of CTX (200 mg/kg) significantly weakened LTP in CA3-CA1 synapses. As shown by elect

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Stoffel, Wilhelm, Jürgen Sasse, Maria Düker, et al. "Human high affinity, Na+ -dependent l -glutamate/l -aspartate transporter GLAST-1 (EAAT-1) : gene structure and localization to chromosome 5p11-p12." FEBS Letters 386, no. 2-3 (1996): 189–93. http://dx.doi.org/10.1016/0014-5793(96)00424-3.

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Kakoki, Masao, Hyung-Suk Kim, Cora-Jean S. Edgell, Nobuyo Maeda, Oliver Smithies, and David L. Mattson. "Amino acids as modulators of endothelium-derived nitric oxide." American Journal of Physiology-Renal Physiology 291, no. 2 (2006): F297—F304. http://dx.doi.org/10.1152/ajprenal.00417.2005.

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To examine the mechanisms whereby amino acids modulate nitric oxide (NO) production and blood flow in the renal vasculature, chemiluminescence techniques were used to quantify NO in the renal venous effluent of the isolated, perfused rat kidney as different amino acids were added to the perfusate. The addition of 10−4 or 10−3 M cationic amino acids (l-ornithine, l-lysine, or l-homoarginine) or neutral amino acids (l-glutamine, l-leucine, or l-serine) to the perfusate decreased NO and increased renal vascular resistance. Perfusion with anionic amino acids (l-glutamate or l-aspartate) had no eff

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Zike, Isaac D., Muhammad O. Chohan, Jared M. Kopelman, et al. "OCD candidate gene SLC1A1/EAAT3 impacts basal ganglia-mediated activity and stereotypic behavior." Proceedings of the National Academy of Sciences 114, no. 22 (2017): 5719–24. http://dx.doi.org/10.1073/pnas.1701736114.

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Obsessive-compulsive disorder (OCD) is a chronic, disabling condition with inadequate treatment options that leave most patients with substantial residual symptoms. Structural, neurochemical, and behavioral findings point to a significant role for basal ganglia circuits and for the glutamate system in OCD. Genetic linkage and association studies in OCD point to SLC1A1, which encodes the neuronal glutamate/aspartate/cysteine transporter excitatory amino acid transporter 3 (EAAT3)/excitatory amino acid transporter 1 (EAAC1). However, no previous studies have investigated EAAT3 in basal ganglia c

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Shuvarikov, Andrey A., Michael Davis, Katharina Esser-Nobis, Sean White, and Michael Gale. "Citrin, a mitochondrial transporter, interacts with NLRP3 and regulates inflammasome activity." Journal of Immunology 206, no. 1_Supplement (2021): 15.16. http://dx.doi.org/10.4049/jimmunol.206.supp.15.16.

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Abstract The NLRP3 protein is a key initiator of inflammation in humans. NLRP3 becomes activated by a multitude of danger signals, including microbial infection, metabolic dysfunction, and cell-internalized particulates. Upon activation, NLRP3 nucleates formation of a multiprotein complex called the inflammasome, in which caspase-1 activity mediates processing of the pro-inflammatory cytokines IL-1β and IL-18 and induces pyroptosis, a pro-inflammatory form of cell death. While multiple regulators of the NLRP3 inflammasome have been described, specific ligands of NLRP3 and its mechanism of acti

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Sharma, Raj Kumar, Santosh Kumar Bharti, Balaji Krishnamachary, et al. "Abstract 6353: Metabolic changes in the spleen and pancreas induced by PDAC xenografts with or without glutamine transporter downregulation." Cancer Research 82, no. 12_Supplement (2022): 6353. http://dx.doi.org/10.1158/1538-7445.am2022-6353.

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Abstract Introduction: Our ongoing studies are focused on characterizing metabolic changes induced in the organs of mice with cachexia-inducing Pa04C human pancreatic cancer xenografts. Because pancreatic cancer cells are glutamine dependent [1], we downregulated the glutamine transporter SLC1A5 in Pa04C cells to determine if metabolic changes induced in the spleen and pancreas by Pa04C tumors were normalized when SLC1A5 was downregulated in these tumors. Metabolic patterns were characterized using high-resolution quantitative 1H magnetic resonance spectroscopy (MRS) of spleen and pancreas tis

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Basuchaudhuri, P. "Genetic aspects of nitrogen metabolism in barley (Hordeum vulgare L.)." International Journal of Multidisciplinary Research and Growth Evaluation 5, no. 4 (2024): 1006–22. http://dx.doi.org/10.54660/.ijmrge.2024.5.4.1006-1022.

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Barley (Hordeum vulgare L.) is gaining a place among cereals as a food and feed for human and animal respectively in recent time because of its nutritive and malting properties. It is known that the crop can be grown efficiently even under harsh environment due to genetic makeup. Nitrogen an essential nutrient influences the growth and yield of barley. Among the constraints under this condition are water and nutrient, especially nitrogen availability. Therefore, an attempt has been made to understand the genetics of nitrogen metabolism vis-à-vis nitrogen utilization efficiency (NUE), nitrogen

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Acton, David, and Gareth B. Miles. "Differential regulation of NMDA receptors by d-serine and glycine in mammalian spinal locomotor networks." Journal of Neurophysiology 117, no. 5 (2017): 1877–93. http://dx.doi.org/10.1152/jn.00810.2016.

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Activation of N-methyl-d-aspartate receptors (NMDARs) requires the binding of a coagonist, either d-serine or glycine, in addition to glutamate. Changes in occupancy of the coagonist binding site are proposed to modulate neural networks including those controlling swimming in frog tadpoles. Here, we characterize regulation of the NMDAR coagonist binding site in mammalian spinal locomotor networks. Blockade of NMDARs by d(−)-2-amino-5-phosphonopentanoic acid (d-APV) or 5,7-dichlorokynurenic acid reduced the frequency and amplitude of pharmacologically induced locomotor-related activity recorded

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Munck, Bjarne Gyldenløve, and Lars Kristian Munck. "Effects of pH changes on systems ASC and B in rabbit ileum." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 1 (1999): G173—G184. http://dx.doi.org/10.1152/ajpgi.1999.276.1.g173.

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Influx ofd-aspartate (d-Asp),l-glutamate (l-Glu), and serine (Ser) across the brush-border membrane of the intact mucosa from rabbit ileum has been examined. l-Glu influx is chloride independent and completely sodium dependent.d-Asp andl-Glu share a transport system with a maximum transport rate of 1 μmol ⋅ cm−2 ⋅ h−1and an apparent affinity constant ( K ½) of ∼0.3 mM. The function of this transport system is pH insensitive between pH 5.65 and 8.2, and bipolar amino acids do not affect the way in which the transport system handlesd-Asp andl-Glu. The characteristics of this transport system mat

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Teichman, Shlomit, and Baruch I. Kanner. "Aspartate-444 Is Essential for Productive Substrate Interactions in a Neuronal Glutamate Transporter." Journal of General Physiology 129, no. 6 (2007): 527–39. http://dx.doi.org/10.1085/jgp.200609707.

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In the central nervous system, electrogenic sodium- and potassium-coupled glutamate transporters terminate the synaptic actions of this neurotransmitter. In contrast to acidic amino acids, dicarboxylic acids are not recognized by glutamate transporters, but the related bacterial DctA transporters are capable of transporting succinate and other dicarboxylic acids. Transmembrane domain 8 contains several residues that differ between these two types of transporters. One of these, aspartate-444 of the neuronal glutamate transporter EAAC1, is conserved in glutamate transporters, but a serine residu

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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.

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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

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Chiu, Martina, Denise Toscani, Emanuela Vicario, et al. "Glutamine Depletion By Addicted Myeloma Cells Inhibits Osteoblastic Differentiation of Bone Marrow Mesenchymal Stromal Cells Limiting Asparagine Availability: A Possible New Mechanism for Myeloma Bone Disease." Blood 134, Supplement_1 (2019): 4339. http://dx.doi.org/10.1182/blood-2019-128034.

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Metabolic alterations of cancer cells, aimed at sustaining their growth, may also influence the behavior of the tumor microenvironment. Our group has recently demonstrated that multiple myeloma (MM) is a highly glutamine(Gln)-addicted tumor that utilize huge amounts of Gln to fuel its metabolism through the enzyme glutaminase (GLS). For this reason, MM cells exhibits increased Gln uptake, mainly through the ASCT2 transporter. Interestingly, lower bone marrow (BM) plasma Gln concentration (down to a median value of 0.4 mM vs. a median value of 0.6 mM) was found in MM patients as compared with s

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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.

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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

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Bridges, Richard J., Michael P. Kavanaugh, and A. Richard Chamberlin. "A Pharmacological Review of Competitive Inhibitors and Substrates of High-affinity, Sodium-dependent Glutamate Transport in the Central Nervous System." Current Pharmaceutical Design 5, no. 5 (1999): 363–79. http://dx.doi.org/10.2174/138161280505230110101259.

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Abstract: The acidic amino acid L-glutamate ucts as both a primary excitatory neurotransmitter and a potential neurotoxin within the mammalian central nervous system. Functionally juxtaposed between these neurophysiological and pathological actions are un assorted group of integral membrane transporter proteins that rapidly and efficiently sequester glutamate into cellular and subcellular compartments. While multiple systems exist that are capable of mediating the uptake or L-glutamate, the high-affinity, sodium-dependent transporters have emerged as the most prominent players in the CNS with

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Hoeltzli, S. D., L. K. Kelley, A. J. Moe, and C. H. Smith. "Anionic amino acid transport systems in isolated basal plasma membrane of human placenta." American Journal of Physiology-Cell Physiology 259, no. 1 (1990): C47—C55. http://dx.doi.org/10.1152/ajpcell.1990.259.1.c47.

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The placenta absorbs anionic amino acids from the maternal and fetal circulations but does not significantly transfer these amino acids from mother to fetus. Uptake of L-aspartate and L-glutamate by basal (fetal-facing) plasma membrane vesicles from placental syncytiotrophoblast was stimulated by an inward sodium and an outward potassium gradient. Measurable saturable uptake was entirely sodium dependent and electrogenic. Studies of concentration dependence resolved a high-affinity (microM) system that has characteristics of the X-AG system found in other tissues including the placental microv

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Peddie, Catherine J., Gregory M. Cook, and Hugh W. Morgan. "Sodium-Dependent Glutamate Uptake by an Alkaliphilic, Thermophilic Bacillus Strain, TA2.A1." Journal of Bacteriology 181, no. 10 (1999): 3172–77. http://dx.doi.org/10.1128/jb.181.10.3172-3177.1999.

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ABSTRACT A strain of Bacillus designated TA2.A1, isolated from a thermal spring in Te Aroha, New Zealand, grew optimally at pH 9.2 and 70°C. Bacillus strain TA2.A1 utilized glutamate as a sole carbon and energy source for growth, and sodium chloride (>5 mM) was an obligate requirement for growth. Growth on glutamate was inhibited by monensin and amiloride, both inhibitors that collapse the sodium gradient (ΔpNa) across the cell membrane.N,N-Dicyclohexylcarbodiimide inhibited the growth of Bacillus strain TA2.A1, suggesting that an F1F0-ATPase (H type) was being used to generate cellular ATP

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Nagamori, Shushi, Pattama Wiriyasermkul, Meritxell Espino Guarch, et al. "Novel cystine transporter in renal proximal tubule identified as a missing partner of cystinuria-related plasma membrane protein rBAT/SLC3A1." Proceedings of the National Academy of Sciences 113, no. 3 (2016): 775–80. http://dx.doi.org/10.1073/pnas.1519959113.

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Heterodimeric amino acid transporters play crucial roles in epithelial transport, as well as in cellular nutrition. Among them, the heterodimer of a membrane protein b0,+AT/SLC7A9 and its auxiliary subunit rBAT/SLC3A1 is responsible for cystine reabsorption in renal proximal tubules. The mutations in either subunit cause cystinuria, an inherited amino aciduria with impaired renal reabsorption of cystine and dibasic amino acids. However, an unsolved paradox is that rBAT is highly expressed in the S3 segment, the late proximal tubules, whereas b0,+AT expression is highest in the S1 segment, the

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Sato, Kota, Mutsumi Inaba, Yuki Suwa, et al. "Inherited Defects of Sodium-dependent Glutamate Transport Mediated by Glutamate/Aspartate Transporter in Canine Red Cells Due to a Decreased Level of Transporter Protein Expression." Journal of Biological Chemistry 275, no. 9 (2000): 6620–27. http://dx.doi.org/10.1074/jbc.275.9.6620.

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Dashper, S. G., L. Brownfield, N. Slakeski, P. S. Zilm, A. H. Rogers, and E. C. Reynolds. "Sodium Ion-Driven Serine/Threonine Transport in Porphyromonas gingivalis." Journal of Bacteriology 183, no. 14 (2001): 4142–48. http://dx.doi.org/10.1128/jb.183.14.4142-4148.2001.

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ABSTRACT Porphyromonas gingivalis is an asaccharolytic, gram-negative bacterium that relies on the fermentation of amino acids for metabolic energy. When grown in continuous culture in complex medium containing 4 mM (each) free serine, threonine, and arginine,P. gingivalis assimilated mainly glutamate/glutamine, serine, threonine, aspartate/asparagine, and leucine in free and/or peptide form. Serine and threonine were assimilated in approximately equal amounts in free and peptide form. We characterized serine transport in this bacterium by measuring uptake of the radiolabeled amino acid in was

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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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Gaal, Lubor, Botond Roska, Serge A. Picaud, Samuel M. Wu, Robert Marc, and Frank S. Werblin. "Postsynaptic Response Kinetics Are Controlled by a Glutamate Transporter at Cone Photoreceptors." Journal of Neurophysiology 79, no. 1 (1998): 190–96. http://dx.doi.org/10.1152/jn.1998.79.1.190.

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Gaal, Lubor, Botond Roska, Serge A. Picaud, Samuel M. Wu, Robert Marc, and Frank S. Werblin. Postsynaptic response kinetics are controlled by a glutamate transporter at cone photoreceptors. J. Neurophysiol. 79: 190–196, 1998. We evaluated the role of the sodium/glutamate transporter at the synaptic terminals of cone photoreceptors in controlling postsynaptic response kinetics. The strategy was to measure the changes in horizontal cell response rate induced by blocking transporter uptake in cones with dihydrokainate (DHK). DHK was chosen as the uptake blocker because, as we show through autorad

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Schwindt, P. C., and W. E. Crill. "Amplification of synaptic current by persistent sodium conductance in apical dendrite of neocortical neurons." Journal of Neurophysiology 74, no. 5 (1995): 2220–24. http://dx.doi.org/10.1152/jn.1995.74.5.2220.

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1. Evidence for amplification of synaptic current by voltage-gated channels in dendrites of neocortical pyramidal neurons was demonstrated by examining the effect of specific channel blocking agents on the current arriving at the soma during iontophoresis of glutamate at a distal site on the apical dendrite. 2. Dendritic noninactivating Na+ channels were implicated in this voltage-dependent amplification of the transmitted current because it was maintained for > 1 s and because tetrodotoxin (TTX) eliminated much of this amplification. 3. Specific blockers of N-methyl-D-aspartate (NMDA) glut

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Kanner, B. I. "Sodium-coupled neurotransmitter transport: structure, function and regulation." Journal of Experimental Biology 196, no. 1 (1994): 237–49. http://dx.doi.org/10.1242/jeb.196.1.237.

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The removal of neurotransmitters by their transporters--located in the plasma membranes of nerve terminals and glial cells--plays an important role in the termination of synaptic transmission. In the last 3 years, many neurotransmitter transporters have been cloned. Structurally and functionally they can be divided into two groups: glutamate transporters, of which to date three have been cloned, couple the flow of glutamate to that of sodium and potassium. The second group of transporters includes those for GABA, glycine, taurine, norepinephrine, dopamine and serotonin. They are sodium- and ch

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