Bibliografie tematiche / Glutamate

Letteratura scientifica selezionata sul tema "Glutamate"

Autore: Grafiati
Pubblicato: 4 giugno 2021
Ultima modifica: 7 luglio 2024

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Articoli di riviste sul tema "Glutamate"

1

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.

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Abstract (sommario):
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 transporters and glutamine synthetase. In this review, we describe the present knowledge concerning the retinal glutamate metabolism under the physiological and pathological conditions.
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2

Matthews, D. E., M. A. Marano e R. G. Campbell. "Splanchnic bed utilization of glutamine and glutamic acid in humans". American Journal of Physiology-Endocrinology and Metabolism 264, n. 6 (1 giugno 1993): E848—E854. http://dx.doi.org/10.1152/ajpendo.1993.264.6.e848.

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Abstract (sommario):
To study the fate of enterally delivered nonessential amino acids, glutamine and glutamate, 14 healthy adults were infused in the postabsorptive state with [2-15N]glutamine and [15N]glutamate for 7 h by intravenous (iv) and nasogastric (ng) tube routes. The amount of enterally delivered tracer that was sequestered by the splanchnic bed on the first pass was 54 +/- 4 and 88 +/- 2% for the [2-15N]glutamine and [15N]glutamate tracers, respectively. Only 46 and 12% of the ng glutamine and glutamate tracers entered systemic blood, respectively. The relative amount of 15N transferred from glutamate to glutamine, the transaminating amino acids leucine, isoleucine, valine, and alanine, and to proline was significantly higher when the [15N]glutamate was infused by the ng vs. iv route. The same was also true for [2-15N]glutamine, which presumably transferred 15N after it was converted to glutamate. Thus we conclude that the splanchnic bed sequesters over one-half of the glutamine and almost all of the glutamate delivered to it in the postabsorptive state. There is production of transaminating amino acids in the splanchnic bed, and the splanchnic bed produces simultaneously both glutamine from glutamate and glutamate from glutamine.
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3

Welbourne, Tomas, e Itzhak Nissim. "Regulation of mitochondrial glutamine/glutamate metabolism by glutamate transport: studies with 15N". American Journal of Physiology-Cell Physiology 280, n. 5 (1 maggio 2001): C1151—C1159. http://dx.doi.org/10.1152/ajpcell.2001.280.5.c1151.

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Abstract (sommario):
We focused on the role of plasma membrane glutamate uptake in modulating the intracellular glutaminase (GA) and glutamate dehydrogenase (GDH) flux and in determining the fate of the intracellular glutamate in the proximal tubule-like LLC-PK1-F+ cell line. We used high-affinity glutamate transport inhibitors d-aspartate (d-Asp) and dl-threo-β-hydroxyaspartate (THA) to block extracellular uptake and then used [15N]glutamate or [2-15N]glutamine to follow the metabolic fate and distribution of glutamine and glutamate. In monolayers incubated with [2-15N]glutamine (99 atom %excess), glutamine and glutamate equilibrated throughout the intra- and extracellular compartments. In the presence of 5 mMd-Asp and 0.5 mM THA, glutamine distribution remained unchanged, but the intracellular glutamate enrichment decreased by 33% ( P < 0.05) as the extracellular enrichment increased by 39% ( P < 0.005). With glutamate uptake blocked, intracellular glutamate concentration decreased by 37% ( P < 0.0001), in contrast to intracellular glutamine concentration, which remained unchanged. Both glutamine disappearance from the media and the estimated intracellular GA flux increased with the fall in the intracellular glutamate concentration. The labeled glutamate and NH[Formula: see text] formed from [2-15N]glutamine and recovered in the media increased 12- and 3-fold, respectively, consistent with accelerated GA and GDH flux. However, labeled alanine formation was reduced by 37%, indicating inhibition of transamination. Although both d-Asp and THA alone accelerated the GA and GDH flux, only THA inhibited transamination. These results are consistent with glutamate transport both regulating and being regulated by glutamine and glutamate metabolism in epithelial cells.
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4

Darmaun, D., D. E. Matthews e D. M. Bier. "Glutamine and glutamate kinetics in humans". American Journal of Physiology-Endocrinology and Metabolism 251, n. 1 (1 luglio 1986): E117—E126. http://dx.doi.org/10.1152/ajpendo.1986.251.1.e117.

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Abstract (sommario):
To study glutamate and glutamine kinetics, 4-h unprimed intravenous infusions of L-[15N]glutamate, L-[2-15N]glutamine, and L-[5-15N]-glutamine were administered to healthy young adult male subjects in the postabsorptive state. Arterialized-venous blood samples were drawn and analyzed for glutamate and glutamine 15N enrichments. The fractional turnover rates of the tracer-miscible glutamate and glutamine pools were fast, 8.0 and 2.8% min-1, respectively. The glutamate tracer-miscible pool accounted for less than one-tenth the estimated free glutamate pool in the body. The plasma glutamate amino N, glutamine amino N and glutamine amide N rates of appearance were 83 +/- 22 (means +/- SD), 348 +/- 33, and 283 +/- 31 mumol X kg-1 X h-1, respectively. The glutamine amide N appearance rate was 20% slower than the amino N appearance rate, indicating that glutamine transaminase is an active pathway in human glutamine metabolism. From measurement of transfer of tracer 15N, we found that only 5% of the glutamine synthesized in cells and released into plasma was derived from intracellular glutamate that had mixed with plasma. These data demonstrate that intravenously administered tracers of glutamate or glutamine do not mix thoroughly with the intracellular pools, and their measured kinetics reflect transport rates through plasma rather than whole-body fluxes.
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5

Welbourne, T. C., K. Horton e M. J. Cronin. "Growth hormone and renal glutamine and glutamate handling." Journal of the American Society of Nephrology 2, n. 7 (gennaio 1992): 1171–77. http://dx.doi.org/10.1681/asn.v271171.

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Abstract (sommario):
Growth hormone administration effects a positive nitrogen balance in part by recycling glutamine nitrogen as glutamate at the expense of ureagenesis. The study presented here focuses on the response of the isolated perfused hypophysectomized rat kidney to acute growth hormone administration during infusions of either glutamine or glutamate. Growth hormone at 50 nM acutely decreases the renal utilization of both glutamine and glutamate while enhancing reabsorption of the latter. During glutamine infusions of either 1,000 or 500 nmol/min, growth hormone markedly reduced net glutamine utilization by 55% at the high loads and reversed utilization to release at the lower load; associated with decreased glutamine utilization was reduced ammonium production and increased glutamate release. Although glutamine reabsorption was unchanged, glutamate reabsorption increased and NH4+ excretion decreased. During glutamate infusion of 180 nmol/min, growth hormone reduced glutamate utilization 66%, the residual utilization matching increased glutamate reabsorption was associated with enhanced bicarbonate reabsorption and a redistribution of NH4+ release into the urine; all three responses were eliminated by amiloride. These responses to growth hormone are consonant with reduced glutamate oxidation underlying decreased glutamine utilization and accelerated luminal Na+-H+ exchange mediating luminal transport, events that are conceivably interrelated.
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6

Vaughn, P. R., C. Lobo, F. C. Battaglia, P. V. Fennessey, R. B. Wilkening e G. Meschia. "Glutamine-glutamate exchange between placenta and fetal liver". American Journal of Physiology-Endocrinology and Metabolism 268, n. 4 (1 aprile 1995): E705—E711. http://dx.doi.org/10.1152/ajpendo.1995.268.4.e705.

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Abstract (sommario):
The hypothesis that glutamine shuttles nitrogen between placenta and fetal liver via interconversion with glutamate was explored by infusing L-[1,2-13C2]glutamine in six fetal sheep chronically catheterized for sampling of the umbilical and hepatic circulations. Fetal plasma glutamine disposal rate was 19.9 +/- 1.3 mumol.min-1.kg fetus-1. Entry of glutamine from the placenta accounted for approximately 60% of the total glutamine entry rate in fetal plasma. Glutamine was taken up by fetal liver, and 45.3 +/- 7.9% of the glutamine taken up was released as glutamate. The fetal liver released large quantities of glutamate, as evidenced by a sixfold increase in plasma glutamate concentration in the blood flowing through the left hepatic lobe and a hepatic glutamate output-to-O2 uptake molar ratio of 0.149 +/- 0.013. In conjunction with a previous study of fetal glutamate metabolism, these data demonstrate that glutamine entering the fetal circulation is converted to glutamate by the fetal liver at a rate of approximately 3-4 mumol.min-1.kg fetus-1.
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7

Nissim, I., B. States, M. Yudkoff e S. Segal. "Characterization of amino acid metabolism by cultured rat kidney cells: study with 15N". American Journal of Physiology-Renal Physiology 253, n. 6 (1 dicembre 1987): F1243—F1252. http://dx.doi.org/10.1152/ajprenal.1987.253.6.f1243.

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Abstract (sommario):
The present study evaluates the metabolism of glutamine and glutamate by normal rat kidney (NRK) cells. The major aim was to evaluate the effect of acute acidosis on the metabolism of amino acid and ammonia formation by cultured NRK cells. Experiments at either pH 7.0 or 7.4 were conducted with phosphate-buffered saline supplemented with either 1 mM [5-15N]glutamine, [2-15N]glutamine, or [15N]glutamate. Incubation with either glutamine or glutamate as a precursor showed that production of ammonia and glucose was increased significantly at pH 7.0 vs. 7.4. The disappearance [corrected] of glutamine and glutamate was linear during a 60-min incubation at either pH. In experiments with [5-15N]glutamine, we found that approximately 57 and 43% of ammonia N was derived from 5-N of glutamine at pH 7.4 and 7.0, respectively. Experiments with [2-15N]glutamine or [15N]glutamate indicated that approximately 43 and 47% of 2-N glutamine and glutamate N utilization, respectively, was accounted for by ammonia production at pH 7.0. Similarly, 28 and 29% of NH3 was derived from 2-N of glutamine or glutamate N by activity of glutamate dehydrogenase at pH 7.4. In addition to 15NH3 formation, three major metabolic pathways of [2-15N]glutamine or [15N]glutamate disposal were identified: 1) transamination reactions involving the pH-independent formation of [15N] aspartate and [15N]alanine; 2) the synthesis of [6-15NH2]adenine nucleotide, a process more active at pH 7.4 vs. 7.0; and 3) glutamine synthesis from [15N]glutamate, especially at pH 7.4. The data indicate that NRK cells in culture consume glutamine and glutamate and generate ammonia and various amino acids, depending on the H+ concentration in the media. The studies suggest that these cell lines may provide a useful model for studying various aspects of the effect of pH on rat renal ammoniagenesis.
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8

Low, S. Y., P. M. Taylor, H. S. Hundal, C. I. Pogson e 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, n. 2 (1 giugno 1992): 333–40. http://dx.doi.org/10.1042/bj2840333.

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Abstract (sommario):
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]glutamate uptake was largely Na(+)-independent. Vmax. values for Na(+)-dependent uptake of glutamine and/or glutamate exceeded control values (by about 2- and 12-fold respectively) in liver membrane vesicles from starved (glutamine), diabetic (glutamate) or steroid-treated (glutamine and glutamate) rats. The Km values for Na(+)-dependent transport of glutamine or glutamate and the rates of their Na(+)-independent uptake were not significantly altered by any treatment. Na(+)-independent glutamate uptake appeared to include a dicarboxylate-exchange component. The patterns of inhibition of glutamine and glutamate uptake by other amino acids indicated that the apparent induction of Na(+)-dependent amino acid transport in catabolic states included increased functional expression of systems A, N (both for glutamine) and X-ag (for glutamate). The results demonstrate that conditions resulting in increased secretion of catabolic hormones (e.g. corticosteroid, glucagon) are associated with increased capacity for Na(+)-dependent transport of amino acids into liver cells from the blood. The modulation of hepatic permeability to glutamine and glutamate in these situations may control the availability of amino acids for intrahepatic metabolic processes such as ureagenesis, ammonia detoxification and gluconeogenesis.
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9

Ta, T. C., F. D. H. Macdowall, M. A. Faris e K. W. Joy. "Metabolism of nitrogen fixed by root nodules of alfalfa (Medicago sativa L.): I. Utilization of [14C, 15N]glutamate and [14C, 15N]glutamine in the synthesis of γ-aminobutyrate". Biochemistry and Cell Biology 66, n. 12 (1 dicembre 1988): 1342–48. http://dx.doi.org/10.1139/o88-155.

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Abstract (sommario):
The fate of nitrogen and carbon from [14C, 15N]glutamate and glutamine, two primary assimilation products of ammonia from fixed nitrogen, was studied by vacuum infiltration of the compounds into alfalfa nodule slices. The amide group of glutamine is an important precursor in the synthesis of asparagine, a major transport compound in alfalfa; this reaction, catalyzed by asparagine synthetase, also produces glutamate. Glutamate is also synthesized by the action of glutamate synthase. Transamination plays an important role in the redistribution of the nitrogen groups to yield a range of amino acids. The rapid transfer of 15N from glutamate to aspartate provides the substrate for asparagine synthesis. Some glutamate was used in glutamine synthesis, indicating the operation of glutamine synthetase. Glutamate is also metabolized by decarboxylation to γ-aminobutyric acid (Gaba), a nonprotein amino acid abundant in alfalfa nodules; Gaba is further metabolized by transamination. Considerable amounts of carbon from both glutamine and glutamate enter the pool of organic acids and are utilized in the synthesis of amino acids. There is relatively little metabolism of glutamate by isolated bacteroids.
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10

Moores, R. R., P. R. Vaughn, F. C. Battaglia, P. V. Fennessey, R. B. Wilkening e G. Meschia. "Glutamate metabolism in fetus and placenta of late-gestation sheep". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 267, n. 1 (1 luglio 1994): R89—R96. http://dx.doi.org/10.1152/ajpregu.1994.267.1.r89.

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Abstract (sommario):
Glutamate is produced by the fetal liver and taken up by the placenta. To explore the functional meaning of this exchange, the disposal rate (DR), clearance, conversion to glutamine, and decarboxylation rate of fetal plasma glutamate were studied at 129 +/- 2 days of gestation in seven fetal lambs infused via a systemic vein with L-[2,3,3,4,4-2H5]glutamate and L-[1-14C]glutamate. In two experiments, L-[1-13C]glutamate was also infused. The mean glutamate DR and clearance were 11.9 +/- 1.3 mumol.min-1.kg-1 and 200 +/- 8 ml.min-1.kg-1, respectively. The placenta extracted 88.5 +/- 0.8% of the tracer glutamate carried by the umbilical circulation and contributed to 61.3 +/- 3.2% of the glutamate DR. Most of the 14C infused as L-[1-14C]glutamate was converted to 14CO2: 37 +/- 4% by the fetus and 41 +/- 6% by the placenta. Of the labeled glutamate taken up by the placenta, 6.2 +/- 1.5% was returned to the fetus as glutamine. The glutamine-to-glutamate enrichment ratio in fetal arterial plasma was 0.066 +/- 0.008. We conclude that fetal plasma glutamate has an exceptionally high clearance because the flux of glutamate into the placenta is virtually equal to umbilical glutamate delivery rate. The main pathway of fetal plasma glutamate disposal is oxidation by placental and fetal tissues. Placental conversion of glutamate to fetal glutamine is a relatively small component of the placental metabolism of fetal glutamate.
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Più fonti

Tesi sul tema "Glutamate"

1

Boulland, Jean-Luc. "Recycling the amino acid neurotransmitter glutamate in the CNS : l'alchimie du glutamate et de la glutamine". Paris 6, 2004. http://www.theses.fr/2004PA066017.

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2

Cabré, Segura Gisela. "New photopharmacological tools for the light-induced control of neuronal signalling". Doctoral thesis, Universitat Autònoma de Barcelona, 2019. http://hdl.handle.net/10803/668303.

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Abstract (sommario):
L’objectiu principal de la neurociència és l’estudi i el control dels sistemes neuronals. Actualment, aquesta àrea està sent revolucionada per l’ús de petites molècules fotoactives, un camp conegut com fotofarmacologia. Mitjançant l’activació remota de fàrmacs amb llum, la fotofarmacologia tracta d’afrontar alguns dels principals reptes de la farmacologia convencional, com la pobra selectivitat dels fàrmacs i els efectes secundaris.1 Tres estratègies principals s’han derivat en aquest camp: els photocaged ligands (CL), profàrmacs que difonen lliurement, l’efecte des quals s’activa mitjançant l’eliminació dels grups protectors fotolàbils amb il·luminació; els photochromic ligands (PCL), que permeten la modulació reversible de la resposta de molècules bioactives a través de la fotoisomerització de grups annexats a aquestes que responen a la llum; i photoswitched tethered ligands (PTL), un cas especial de PCLs que s'uneixen covalentment al receptor d’interès. Tot i que aquestes aproximacions han demostrat tenir èxit per a una gran varietat d’objectius terapèutics, tant in vitro com in vivo, encara resten diversos reptes en el camp de la fotofarmacologia. Per tant, en aquest treball hem abordat la investigació de noves estratègies fotofarmacològiques que superin algunes de les debilitats de les eines desenvolupades fins ara. Ens hem centrat especialment en el fotocontrol dels receptors ionotròpics de glutamat (iGluRs), els quals tenen un paper clau en la modulació de l’excitabilitat neuronal. Les noves eines fotofarmacològiques desenvolupades al llarg d’aquesta tesi consisteixen en: (i) un PTL basat en fotointerruptors basats en azobenzè substituïts de forma push-pull que responen a l'excitació amb dos fotons amb llum NIR. (ii) un lligand engabiat no destructiu que permeti la conversió irreversible i quantitativa de l'estat inactiu a l'estat actiu, actuant d'una manera similar als CLs, però sense generació de subproductes. (iii) un PCL basat en azobenzens amb un pont C2 que presenta una forma inactiva termodinàmicament estable que es converteix selectivament en l’estat biològicament actiu al ser irradiat. Aquesta tesi presenta la síntesi, la caracterització fotoquímica i l’avaluació de l’activitat biològica d’aquestes tres noves eines fotofarmacològiques.
The main objective of neuroscience is the study and control of neuronal systems. Nowadays, this area is being revolutionised by the use of photoresponsive small molecules, a field known as photopharmacology. By enabling remote activation of drugs with light, photopharmacology seeks to tackle some of the main challenges faced by conventional pharmacology, such as poor drug selectivity and side effects.1 Three main strategies have been derived in this area: photocaged ligands (CL), freely diffusing prodrugs the effect of which is triggered by removing photolabile protecting groups upon illumination; photochromic ligands (PCL), which allow reversible modulation of the response of bioactive molecules through photoisomerisation of appended light-responsive moieties; and photoswitched tethered ligands (PTL), a special case of PCLs that are covalently attached to the therapeutic receptor. Although these approaches have proven to be successful for a variety of therapeutic targets in vitro and in vivo, several challenges still remain in the field of photopharmacology. Therefore, in this work we have aimed at the investigation of new photopharmacological strategies that overcome some of the weaknesses of the tools developed so far. We have particularly focused on the photocontrol of ionotropic glutamate receptors (iGluRs), which play a key role in the modulation of neuronal excitability. The novel photopharmacological tools developed along this thesis consist in: (i) a PTL based on push-pull-substituted azobenzene photoswitches that responds to two-photon excitation with NIR light. (ii) a non-destructive caged ligand that enable irreversible and quantitative conversion from the inactive to the active state, thus performing in a similar fashion as CLs but without by-product generation. (iii) a PCL based on C2-bridged azobenzenes which displays a thermodynamically stable inactive form that selectively turns into the biologically-active state when irradiated. This thesis reports the synthesis, photochemical characterisation and biological activity evaluation of these three novel photopharmacological approaches.
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3

Scott-Taggart, Catherine Patricia. "Inhibition of glutamine production increases glutamate metabolism via the GABA shunt". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ27542.pdf.

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4

Barel, Itai. "The regulation of glutamine synthetase and glutamate synthase in Schizosaccharomyces pombe". Thesis, University of Cambridge, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.279649.

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5

Silva, Jackeline Thaís da. "Aminoácidos limitantes para o desempenho de bezerros leiteiros: avaliação de teores ótimos e via de fornecimento". Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/11/11139/tde-11112014-163521/.

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Abstract (sommario):
O objetivo neste trabalho foi avaliar a concentração de aminoácidos essenciais (Lisina e Metionina) considerada na literatura como ideal, de acordo com a via de fornecimento (sucedâneo ou concentrado inicial), e sua associação com a suplementação de Glutamato e Glutamina, para bezerros em dois sistemas de aleitamento: convencional ou programado. No primeiro experimento foi realizado o levantamento da composição bromatológica e em aminoácidos dos principais sucedâneos comercializados no Brasil. Nos segundo e terceiro experimentos foram utilizados 45 bezerros da raça Holandês, em delineamento de blocos casualizados distribuídos nos tratamentos: 1) Controle: sem suplementação; 2) Suplementação de lisina e metionina para atingir consumo de 17 e 5,3 g/d, respectivamente, com correção feita com base na análise do sucedâneo, 3) Suplementação de lisina e metionina, para atingir consumo de 17 e 5,3 g/d, respectivamente, com correção feita com base na análise do concentrado inicial. A diferença entre os experimentos foi o sistema de aleitamento ao qual os bezerros foram submetidos: no segundo experimento os animais receberam 6L/d de sucedâneo; enquanto no terceiro estudo os animais foram submetidos ao sistema de aleitamento programado (4L/d até a 2ª semana; 8L/d da 3ª a 6ª semana; 4L/d da 7ª a 8ª semana). No quarto experimento o mesmo delineamento foi utilizado para avaliar, em sistema de aleitamento convencional, os tratamentos: 1) Controle: sem suplementação; 2) Sucedâneo lácteo suplementado com Lisina e Metionina, para atingir consumo de 17 e 5,3g/d, respectivamente + 1% na MS de produto contendo 10% de glutamato e de glutamina; 3) Sucedâneo lácteo suplementado com Lisina e Metionina para atingir consumo de 17 e 5,3g/d + 0,6% na MS de produto contendo 10% de glutamato e de glutamina. Os animais foram alojados em abrigos individuais, com livre acesso a água e concentrado inicial. O consumo de concentrado inicial e o escore fecal dos animais foram registrados diariamente. Semanalmente, foram realizadas pesagens e medidas de crescimento corporal. Nas semanas 2, 4, 6, 8 e 10 de vida foram realizadas colheitas de sangue para determinação de metabólitos como marcadores do status protéico dos animais (albumina, proteína total, N-ureico), status energético (glicose e ?-hidroxibutirato), crescimento ósseo (fosfatase alcalina) e crescimento muscular (creatinina). A composição em aminoácidos dos sucedâneos comercializados no Brasil foi menor que o esperado para dieta que substitui o leite integral. Nos experimentos 2 e 3 a suplementação com lisina e metionina no sucedâneo ou no concentrado inicial para bezerros não resultou em benefícios no desempenho ou no metabolismo. No estudo 4, a suplementação do sucedâneo com lisina, metionina em associação com glutamato e glutamina não alterou o desempenho, a saúde intestinal ou o metabolismo de bezerros leiteiros.
The aim in this work was to evaluate the concentration of essential amino acids (Lysine and Methionine) considered in the literature as ideal, according to feeding route (milk replacer or starter concentrate), and its association with the supplementation of glutamate and glutamine to calves in two feeding systems: conventional or step-down. In the first study, the chemical composition was analyzed and in amino acids of main milk replacer marketed in Brazil. In the second and third studies, 45 Holstein calves were used, in randomized blocks distributed in treatments: 1) Control: without supplementation; 2) Supplementation with lysine and methionine to reach consumption of 17 and 5.3 g/d, respectively, with correction based on the analysis basis of the milk replacer, 3) Supplementation of lysine and methionine to reach consumption of 17 and 5.3 g/d, respectively, with correction based on the analysis basis of starter concentrate. The difference between the experiments was the feeding system applied to the calves: in the second study, the animals received 6 L/d of milk replacer; while in the third study, the animals were submitted to the step-down system (4L/d until the 2nd week; 8L/d of the 3nd to 6th week; 4L/d of the 7th to 8th week). In the fourth study, the same experimental design was used to evaluate, in a conventional feeding system, treatments: 1) Control: without supplementation; 2) AminoGut 0.6%: milk replacer supplemented with Lysine and Methionine, to reach consumption 17 and 5.3g/d, respectively + 0.6% product containing 10% of glutamate and glutamine; 3) AminoGut 1%: milk replacer supplemented with Lysine and Methionine to reach consumption 17 and 5.3g/d + 0.6% product containing 10% of glutamate and glutamine. The animals were housed in individual hutches, with free access to water and starter concentrate. The consumption of starter concentrate and fecal scores of animals were monitored daily. Body growth was weighed and measured weekly. In weeks 2, 4, 6, 8 and 10, blood samples were collected to determine the metabolites as markers of protein status of animals (albumin, total protein, N-urea), energy status (glucose and BHBA), bone growth (alkaline phosphatase) and muscular growth (creatinine). The composition of amino acids of the milk replacer marketed in Brazil was lower than expected for diet that replaces the whole milk. In study 2 and 3, the supplementation of the milk replacer or starter concentrate with lysine and methionine resulted in no benefit on dairy calves performance or metabolism. In study 4 the supplementation of the milk replacer with lysine and methionine in association with glutamate and glutmine had no effect on performance, gut health nor metabolism of dairy calves.
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6

Apricò, Karina 1977. "[3H](2S,4R)-4-methylglutamate as a novel radioligand for brain glutamate transporters". Monash University, Dept. of Pharmacology, 2003. http://arrow.monash.edu.au/hdl/1959.1/5497.

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7

Girard, Benoît. "Impact de l’activation du récepteur mGlu7 dans l’épilepsie". Thesis, Montpellier, 2018. http://www.theses.fr/2018MONTT038.

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L'épilepsie affecte des millions de patients dans le monde. Les traitements disponibles sont symptomatiques, ils per récepteur mGlu7 du glutamate dans la modulation non seulement de l’excitabilité, mais également de l'hypersynchronisation des réseaux de neurones, deux facteurs cruciaux dans les crises d'épilepsie. J'ai parachevé ces découvertes qui ont été à l’origine d’une première publication (Tassin, Girard et al. 2016).A l’aide d’un nouvel agoniste du récepteur mGlu7, le LSP2-9166, lors de ma thèse j'ai ensuite étudié l’impact de ce récepteur dans différents modèles d’épilepsie chez la souris. Deux modèles complémentaires ont été utilisés : le kindling (embrasement), modèle chimique induit par le pentylènetétrazol (PTZ) qui sensibilise le cerveau jusqu’à générer des crises tonico-cloniques généralisées, et l’injection intra-hippocampique de kainate, mimant l’épilepsie mésiale du lobe temporal chez l'homme.Dans un premier temps j'ai observé une atténuation de la progression de la sévérité des crises dans le modèle de kindling au PTZ, sous l’activation du récepteur mGlu7. Cet effet a été corrélé à une inflammation, et une activation microgliale et astrocytaire plus faibles. Dans le modèle d’injection intra-hippocampique de KA, considéré comme pharmaco-résistant, l’activation du récepteur mGlu7 pendant la période d’épileptogenèse a augmenté la durée des périodes interictales et diminué la durée des crises ainsi que la réorganisation neuronale. Une fois les crises chroniques installées, l’activation aigu du récepteur mGlu7 a diminué le nombre de crises aussi fortement que le diazépam couramment utilisé dans le cadre clinique. Pour finir, des injections chroniques de LSP2-9166 chez des animaux naïfs (non épileptiques) n’engendrent pas de déficit cognitif ou comportemental détectables, ni de modification du niveau d’ARNm du récepteur mGlu7. L’activation du récepteur mGlu7 offre donc une cible stratégique dans nos deux modèles.Ces travaux permettent une meilleurmettent de traiter les crises sans pour autant éviter la progression de la maladie et présentent de lourds effets secondaires. La découverte de nouvelles cibles thérapeutiques et de nouveaux composés reste primordiale pour dépasser les limites des stratégies thérapeutiques actuelles. Au début de ma thèse, des études précédentes avaient montré une implication due compréhension du rôle du récepteur mGlu7 dans l’épileptogenèse. Ils participent ainsi à la recherche de futurs traitements. antiépileptiques adéquats
Epilepsy affects millions of patients worldwide. The available treatments are symptomatic, they treat seizures without preventing the progression of the disease and have heavy side effects. The discovery of new therapeutic targets and new compounds is therefore essential to overcome the limitations of current therapeutic strategies. Previous studies have demonstrated substantial involvement of the mGlu7 receptor in modulating not only excitability but also hypersynchronization of neural networks, two crucial factors affecting epileptic seizures. These discoveries were at the origin of a first publication that I completed at the beginning of my thesis (Tassin, Girard et al., 2016).Using a new mGlu7 receptor agonist, LSP2-9166, in my thesis I then studied the impact of this receptor in different epilepsy models in mice. Two complementary models were used: kindling, a chemical model induced by pentylenetetrazol (PTZ) which sensitizes the brain to induce generalized tonic-clonic seizures, and intra-hippocampal injection of kainate, mimicking mesial temporal lobe epilepsy in humans.At first, I observed an attenuation of the progression of the seizures severity in the PTZ kindling model, under the activation of the mGlu7 receptor. This effect was correlated with weaker inflammation, and microglial and astrocytic activation. In the intra-hippocampal injection model of KA, considered as drug-resistant, activation of the mGlu7 receptor during the epileptogenesis period increased the duration of interictal periods and decreased the duration of seizures as well as neuronal reorganization. Once chronic seizures were established, acute activation of the mGlu7 receptor decreased the number of seizures as strongly as diazepam, commonly used in clinical settings. Finally, chronic injections of LSP2-9166 into naive (non epileptic) animals do not generate any detectable cognitive or behavioral deficits or changes in mGlu7 receptor mRNA level. The activation of the mGlu7 receptor thus presents a strategic target in our two models.This work provides a better understanding of the role of the mGlu7 receptor in epileptogenesis. It participates in the search for future more adequate treatments
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Sachidhanandam, Shankar. "Rôle des récepteurs kaïnate dans le transfert d'information dans l'hippocampe". Bordeaux 2, 2007. http://www.theses.fr/2007BOR21433.

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Les récepteurs kaïnate (KAR) sont des récepteurs ionotropiques du glutamate impliqués dans la régulation de la transmission synaptique et de l'excitabilité neuronale. Ils sont exprimés au niveau des synapses entre les fibres moussues du gyrus dentelé et les neurones pyramidaux de la région CA3 de l'hippocampe (synapse FM-CA3) dans les domaines pré- et post-synaptiques. En étudiant leurs rôles physiologiques dans le transfert de l'information par ces synapses dans l'hippocampe de souris, nous avons montré que les KAR post-synaptiques agissent de deux manières : par une action ionotropique directe impliquant GluR6 et par un mécanisme indirect métabotropique via un couplage à des protéines G, suite à la liaison du glutamate à KA2. Ceci inhibe transitoirement les courants à l'origine de l'hyperpolarisation lente après activité (IsAHP) et augmente l'excitabilité neuronale. Nous avons aussi pu montrer, en utilisant des souris transgéniques, que les KAR pré- et post-synaptiques agissent de concert pour amplifier les potentiels post-synaptiques excitateurs unitaires, permettant le déclenchement des potentiels d'action (PA) et améliorant leur précision temporelle pour des fréquences entre 3 et 50 Hz. La modulation de IsAHP par KA2 augmente le nombre de PA durant des trains prolongés de stimulations et les KAR permettent l'induction de la potentialisation à long terme des synapses associatives/commissurales. Les rôles des KAR mis en évidence par des stimuli contrôlés sont conservés durant des patrons de décharges physiologiques des fibres moussues afférentes. En conclusion, les KAR agissent comme des amplificateurs de la transmission synaptique FM-CA3
Kainate receptors (KAR) are ionotropic glutamate receptors implicated in the regulation of synaptic transmission and neuronal excitability. At the mossy fiber (Mf) synapse, KARs can be expressed both pre and postsynaptically. In this study, we examined physiological role of KARs in information transfer at the Mf-CA3 pyramidal cell synapse in the mouse hippocampus. We show that KARs can operate in dual mode, by a direct ionotropic action via GluR6, and an indirect G-protein coupled mechanism requiring the binding of glutamate to KA2, to inhibit the slow afterhyperpolarization (IsAHP), hence enhancing neuronal excitability. Using mice deficient for the various KAR subunits, we show that postsynaptic KARs shape the waveform of unitary EPSPs, and pre and postsynaptic KARs act together to amplify unitary EPSPs, triggering spike discharge under conditions of sustained mossy fiber activity. KARs improve timing precision within a frequency range of 3 to 50 Hz and modulation of IsAHP by KA2 facilitates spike discharge in prolonged stimulus trains. KARs are permissive to the induction of LTP at the associative/commissural input. Physiological patterns of afferent input reproduce the output obtained with controlled stimulus inputs. Hence KARs act as amplifiers of synaptic transmission, to enhance the transfer of information at the Mf-CA3 pyramidal cell synapse
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Martin, Emily P. "Expression of glutamate dehydrogenase and glutamine synthetase RNA in preimplantation mouse embryos". Virtual Press, 1999. http://liblink.bsu.edu/uhtbin/catkey/1117849.

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Glutamine serves as a major energy source for all stages of preimplantation mouse embryo development, whether the embryos are raised in vivo or in vitro from the one-cell stage. Glutamate dehydrogenase (GDH) and glutamine synthetase (GS) are enzymes that are involved in the metabolism of glutamine. GDH catalyzes the conversion of glutamate into a-ketoglutarate, a primary component of the tricarboxylic acid cycle. GS catalyzes the conversion of glutamate to glutamine. The expression of GDH RNA and GS RNA were analyzed in preimplantation mouse embryos using reverse transcription (RT) with an oligo dT primer followed by Polymerase Chain Reaction (PCR) amplification of GDH and GS cDNAs using gene specific primers. Data show that GDH RNA is expressed in mouse embryos grown in vivo at the one-cell, two-cell, eight-cell, and blastocyst stages of development. GS RNA is not expressed at the one-cell stage, but first appears at the two-cell stage and is expressed at the eight-cell and blastocyst stages. Semiquantitative PCR analysis using a globin internal standard demonstrated that GS RNA is present at high levels at the two-cell stage and declines by 51 % by the blastocyst stage. These results suggest that, within the preimplantation mouse embryo, GDH RNA is expressed by both the maternal genome as well as the embryonic genome, while GS RNA is only expressed by the embryonic genome. This study provides an explanation for why glutamine is utilized as an energy source during preimplantation development, which allows for a better understanding of glutamine metabolism and its role during early mouse development.
Department of Biology
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Saito, Kelly Cristina. "Envolvimento de Rac1 na excitotoxicidade induzida por NMDA na retina de ratos". Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/42/42134/tde-10022012-132908/.

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A ativação excessiva dos receptores NMDA tem sido descrita no disparo da morte neuronal que ocorre em doenças, como o glaucoma. É possível que a combinação de subunidades (NR2A-D) possa ativar vias de sinalização intracelulares que resultam na morte ou sobrevivência. Nosso objetivo foi investigar o envolvimento de subunidades NR2 e Rac1, membro da família Rho GTPase, na morte de neurônios da retina. A morte induzida por glutamato in vitro foi reduzida após a inibição de Rac1 e bloqueio de NR2B, mas não das subunidades NR2C/D. Resultados semelhantes foram obtidos in vivo após injeção intravítrea NMDA, e a detecção de Rac1 ativo, principalmente, nos processos de glia de Müller foi inibida pelo bloqueio NR2B. Além disso, a produção de TNF-α após a injeção de NMDA foi reduzida pelo bloqueio de NR2B e Rac1. Assim, nossos resultados sugerem que a excitotoxicidade via receptores NR2B/NMDA ativa Rac1 em células da glia de Müller, que por sua vez controla a produção de TNF-α possível responsável pela morte de células ganglionares da retina.
Overactivation of NMDA receptors has been described to trigger neuronal death that occurs in diseases such as glaucoma. It is possible that the combination of subunits (NR2A-D) activate intracellular signaling pathways that result in death or survival. Our aim was to investigate the involvement of NR2 subunits and Rac1, a member of Rho GTPase family, in retinal neuronal death. Glutamate-induced neuronal death in vitro was reduced after Rac1 inhibition and by NR2B blocking, but not NR2C/D subunits. Similar results were obtained in vivo after NMDA intravitreous injection, although active Rac1 was mainly detected in Müller glia processes, and it was inhibited by NR2B blockade. In addition, TNF-α level after NMDA injection were reduced by NR2B blocking and Rac1. Thus, our results suggest that excitotoxicity via NR2B/NMDA receptors activate Rac1 in Müller glia cells, which in turn controls the TNF-α production that triggers retinal ganglion cell death.
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Libri sul tema "Glutamate"

1

Schousboe, Arne, e Ursula Sonnewald, a cura di. The Glutamate/GABA-Glutamine Cycle. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-45096-4.

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Alton, Meister, a cura di. Glutamate, glutamine, glutathione, and related compounds. Orlando, Fla: Academic Press, 1985.

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3

P, Ottersen O., e Storm-Mathisen Jon, a cura di. Glutamate. Amsterdam: Elsevier, 2000.

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Burger, Corinna, e Margaret Jo Velardo, a cura di. Glutamate Receptors. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9077-1.

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Herman, Barbara H., Jerry Frankenheim, Raye Z. Litten, Philip H. Sheridan, Forrest F. Weight e Stephen R. Zukin. Glutamate and Addiction. New Jersey: Humana Press, 2002. http://dx.doi.org/10.1385/1592593062.

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Gereau, Robert W., e Geoffrey T. Swanson, a cura di. The Glutamate Receptors. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-055-3.

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H, Herman Barbara, e Frankenheim Jerry, a cura di. Glutamate and addiction. Totowa, N.J: Humana Press, 2003.

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Baskys, Andrius. Metabotropic glutamate receptors. Austin: R.G. Landes Co., 1994.

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Pavlovic, Zoran M., a cura di. Glutamate and Neuropsychiatric Disorders. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-87480-3.

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Conn, P. Jeffrey, e Jitendra Patel, a cura di. The Metabotropic Glutamate Receptors. Totowa, NJ: Humana Press, 1994. http://dx.doi.org/10.1007/978-1-4757-2298-7.

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Capitoli di libri sul tema "Glutamate"

1

Sanzone, Marla. "Glutamate". In Encyclopedia of Clinical Neuropsychology, 1160–62. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-79948-3_1661.

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Sanzone, Marla. "Glutamate". In Encyclopedia of Clinical Neuropsychology, 1–3. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56782-2_1661-2.

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Sanzone, Marla. "Glutamate". In Encyclopedia of Clinical Neuropsychology, 1587–89. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_1661.

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Manji, Husseini K., Jorge Quiroz, R. Andrew Chambers, Anthony Absalom, David Menon, Patrizia Porcu, A. Leslie Morrow et al. "Glutamate". In Encyclopedia of Psychopharmacology, 559. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_1695.

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Nistri, Andrea. "Glutamate". In Neurotransmitter Actions in the Vertebrate Nervous System, 101–23. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4961-7_4.

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Yuen, Eunice. "Glutamate". In Encyclopedia of Autism Spectrum Disorders, 1–2. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4614-6435-8_102077-1.

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Duce, Ian R. "Glutamate". In Comparative Invertebrate Neurochemistry, 42–89. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4615-9804-6_2.

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Murala, Sireesha, Aditya Boddu e Pradeep C. Bollu. "Glutamate". In Neurochemistry in Clinical Practice, 91–107. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-07897-2_5.

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Yuen, Eunice. "Glutamate". In Encyclopedia of Autism Spectrum Disorders, 2258. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-91280-6_102077.

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Öz, Gülin, David A. Okar e Pierre-Gilles Henry. "Glutamate-Glutamine Cycle and Anaplerosis". In Neural Metabolism In Vivo, 921–46. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4614-1788-0_32.

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Atti di convegni sul tema "Glutamate"

1

Syafiie, S., e I. H. Mustafa. "Single compartment modeling glutamine-glutamate-GABA system in neuron". In 2016 IEEE EMBS Conference on Biomedical Engineering and Sciences (IECBES). IEEE, 2016. http://dx.doi.org/10.1109/iecbes.2016.7843506.

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Rahman, M. M., T. Yamazaki, T. Ikeda, M. Ishida e K. Sawada. "Development of a glutamate biosensor based on glutamate oxidase using smart-biochips". In TRANSDUCERS 2009 - 2009 International Solid-State Sensors, Actuators and Microsystems Conference. IEEE, 2009. http://dx.doi.org/10.1109/sensor.2009.5285556.

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Sakinyte-Urbikiene, Ieva, Vidute Gureviciene e Julija Razumiene. "Amperometric Biosensing of L-Glutamate Using Reduced Graphene Oxide and Glutamate Oxidase". In Eurosensors 2023. Basel Switzerland: MDPI, 2024. http://dx.doi.org/10.3390/proceedings2024097005.

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Macpherson, IR, E. Dornier, N. Rabas, E. Rainero e JC Norman. "Abstract P6-01-06: Glutamine metabolism drives breast cancer invasion by providing a source of extracellular glutamate to activate the GRM3 metabotropic glutamate receptor". In Abstracts: 2016 San Antonio Breast Cancer Symposium; December 6-10, 2016; San Antonio, Texas. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.sabcs16-p6-01-06.

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Bernal-Martínez, Juan. "L-glutamate Receptor In Paramecium". In MEDICAL PHYSICS: Eighth Mexican Symposium on Medical Physics. AIP, 2004. http://dx.doi.org/10.1063/1.1811853.

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Lee, Gija, Seokkeun Choi, Sungwook Kang, Samjin Choi, Jeonghoon Park, Dong Hyun Park, Youngho Park, Kyungsook Kim, Bermseok Oh e Hunkuk Park. "Changes in Extracellular Glutamate Release on Repetitive Transient Occlusion in Global Ischemia Model". In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206602.

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During the operation, surgeons in neurosurgical area usually performed the multiple temporary occlusions of parental artery which may induce the neuronal damage. It is generally thought that neuronal damage by cerebral ischemia is associated with extracellular concentrations of the excitatory amino acids. In this experiment, we measured the dynamics of extracellular glutamate release in 11 vessel occlusion (VO) model during repeated within short interval. Changes in cerebral blood flow were monitored by laser-Doppler flowmetry simultaneously with cortical glutamate level measured by amperometric biosensor. During ischemia, the peak level of glutamate release was gradually decreased as 112.38±26.21 μM in first period, 82.63±18.50 μM in second period, and 48.58±11.89 μM in third period. The time interval between the ischemia induction and the beginning of glutamate release was increased as 106.7 ± 10.89 (sec) at first attack, 139.11 ± 3.87 (sec) in second attack, 169.00 ± 14.56 (sec) in third ischemic period. From the results of real-time monitoring about glutamate release in 11-VO model during repetitive ischemic episode, it was demonstrated that repetitive ischemia induced less glutamate release from neuronal cell than single ischemia due to endogeneous protective mechanism which delayed glutamate release time in later ischemic injury.
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Mohan, A., J. Gall, S. Nair e P. Kalivas. "Glutamate Dynamics in the PFC-NAC Synapse". In ASME 2006 International Mechanical Engineering Congress and Exposition. ASMEDC, 2006. http://dx.doi.org/10.1115/imece2006-15401.

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A computational model of glutamate dynamics in the PFC-NAc syapse is developed. The mechanisms considered are release of glutamate into the synapse, diffusion of synaptic glutamate into the extracellular space, Glu added by cystine-glutamate exchanger, Glu removal via transporters, and binding to mGluR's. The model will be used to determine the relative impact of the different mechanisms on Glu homeostasis, by using information about Glu levels and ranges for the known parameters and kinetic constants. The model will then be integrated with a PFC cell firing model to investigate the effects of cocaine-induced cellular adaptations in the PFC-NAc glutamatergic pathway.
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Kotake, Naoki, Takafumi Suzuki, Osamu Fukayama e Kunihiko Mabuchi. "A flexible parylene-based glutamate sensor". In 5th International IEEE/EMBS Conference on Neural Engineering (NER 2011). IEEE, 2011. http://dx.doi.org/10.1109/ner.2011.5910550.

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Gao, Yong. "UASB Treatment of Monosodium Glutamate Wastewater". In 2010 4th International Conference on Bioinformatics and Biomedical Engineering (iCBBE). IEEE, 2010. http://dx.doi.org/10.1109/icbbe.2010.5516404.

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Xiao, Guihua, Yilin Song, Song Zhang, Shengwei Xu, Lili Yang, Huiren Xu e Xinxia Cai. "Microelectrode arrays studies of glutamate excitatory pathway in hippocampus CA3 by offside KCl and glutamate stimulating". In 2017 8th International IEEE/EMBS Conference on Neural Engineering (NER). IEEE, 2017. http://dx.doi.org/10.1109/ner.2017.8008333.

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Rapporti di organizzazioni sul tema "Glutamate"

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Niu, Li. Glutamate Receptor Aptamers and ALS. Fort Belvoir, VA: Defense Technical Information Center, gennaio 2008. http://dx.doi.org/10.21236/ada481452.

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Risbrough, Victoria. Glutamate Transmission Enhancement for Treatment of PTSD. Fort Belvoir, VA: Defense Technical Information Center, marzo 2009. http://dx.doi.org/10.21236/ada506358.

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Michaelis, Elias K. Molecular Characteristics of Membrane Glutamate Receptor-Ionophore Interaction. Fort Belvoir, VA: Defense Technical Information Center, ottobre 1988. http://dx.doi.org/10.21236/ada201954.

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Surmeier, James. Glutamate Signaling and Mitochnodrial Dysfunction in Models of Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, dicembre 2012. http://dx.doi.org/10.21236/ada602445.

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Surmeier, D. J. Glutamate Signaling and Mitochondrial Dysfunction in Models of Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, marzo 2014. http://dx.doi.org/10.21236/ada604089.

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Stern, Michael. Group II Metabotropic Glutamate Receptors as Potential Pharmaceutical Targets for Neurofibroma Formation. Fort Belvoir, VA: Defense Technical Information Center, febbraio 2010. http://dx.doi.org/10.21236/ada542280.

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Stern, Michael. Group II Metabotropic Glutamate Receptors as Potential Pharmaceutical Targets for Neurofibroma Formation. Fort Belvoir, VA: Defense Technical Information Center, febbraio 2011. http://dx.doi.org/10.21236/ada542347.

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Fromm, Hillel, e Joe Poovaiah. Calcium- and Calmodulin-Mediated Regulation of Plant Responses to Stress. United States Department of Agriculture, settembre 1993. http://dx.doi.org/10.32747/1993.7568096.bard.

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We have taken a molecular approach to clone cellular targets of calcium/calmodulin (Ca2+/CaM). A 35S-labeled recombinant CaM was used as a probe to screen various cDNA expression libraries. One of the isolated clones from petunia codes for the enzyme glutamate decarboxylase (GAD) which catalyzes the conversion of glutamate to g-aminobutyric acid (GABA). The activity of plant GAD has been shown to be dramatically enhanced in response to cold and heat shock, anoxia, drought, mechanical manipulations and by exogenous application of the stress phytohormone ABA in wheat roots. We have purified the recombinant GAD by CaM-affinity chromatography and studied its regulation by Ca2+/CaM. At a physiological pH range (7.0-7.5), the purified enzyme was inactive in the absence of Ca2+ and CaM but could be stimulated to high levels of activity by the addition of exogenous CaM (K0.5 = 15 nM) in the presence of Ca2+ (K 0.5 = 0.8 mM). Neither Ca2+ nor CaM alone had any effect on GAD activity. Transgenic tobacco plants expressing a mutant petunia GAD lacking the CaM-binding domain, or transgenic plants expressing the intact GAD were prepared and studied in detail. We have shown that the CaM-binding domain is necessary for the regulation of glutamate and GABA metabolism and for normal plant development. Moreover, we found that CaM is tightly associated with a 500 kDa GAD complex. The tight association of CaM with its target may be important for the rapid modulation of GAD activity by Ca2+ signaling in response to stresses.
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Akanji, Bukunmi Abongwa. Functional expression of a glutamate-gated chloride channel (GLC-3) from adult Brugia malayi. Ames (Iowa): Iowa State University, gennaio 2018. http://dx.doi.org/10.31274/cc-20240624-771.

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Liu, Ya F. Molecular Analysis of the Common Signaling Mechanism of Neuronal Death Induced by Glutamate and Mutated Huntington. Fort Belvoir, VA: Defense Technical Information Center, marzo 2001. http://dx.doi.org/10.21236/ada393700.

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