Relevant bibliographies by topics / Glutamate and aspartate

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Academic literature on the topic 'Glutamate and aspartate'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Glutamate and aspartate"

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NISSIM, Itzhak, Oksana HORYN, Bohdan LUHOVYY, Adam LAZAROW, Yevgeny DAIKHIN, Ilana NISSIM, and Marc YUDKOFF. "Role of the glutamate dehydrogenase reaction in furnishing aspartate nitrogen for urea synthesis: studies in perfused rat liver with 15N." Biochemical Journal 376, no. 1 (November 15, 2003): 179–88. http://dx.doi.org/10.1042/bj20030997.

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The present study was designed to determine: (i) the role of the reductive amination of α-ketoglutarate via the glutamate dehydrogenase reaction in furnishing mitochondrial glutamate and its transamination into aspartate; (ii) the relative incorporation of perfusate 15NH4Cl, [2-15N]glutamine or [5-15N]glutamine into carbamoyl phosphate and aspartate-N and, thereby, [15N]urea isotopomers; and (iii) the extent to which perfusate [15N]aspartate is taken up by the liver and incorporated into [15N]urea. We used a liver-perfusion system containing a physiological mixture of amino acids and ammonia similar to concentrations in vivo, with 15N label only in glutamine, ammonia or aspartate. The results demonstrate that in perfusions with a physiological mixture of amino acids, approx. 45 and 30% of total urea-N output was derived from perfusate ammonia and glutamine-N respectively. Approximately two-thirds of the ammonia utilized for carbamoyl phosphate synthesis was derived from perfusate ammonia and one-third from glutamine. Perfusate [2-15N]glutamine, [5-15N]glutamine or [15N]aspartate provided 24, 10 and 10% respectively of the hepatic aspartate-N pool, whereas perfusate 15NH4Cl provided approx. 37% of aspartate-N utilized for urea synthesis, secondary to the net formation of [15N]glutamate via the glutamate dehydrogenase reaction. The results suggest that the mitochondrial glutamate formed via the reductive amination of α-ketoglutarate may have a key role in ammonia detoxification by the following processes: (i) furnishing aspartate-N for ureagenesis; (ii) serving as a scavenger for excess ammonia; and (iii) improving the availability of the mitochondrial [glutamate] for synthesis of N-acetylglutamate. In addition, the current findings suggest that the formation of aspartate via the mitochondrial aspartate aminotransferase reaction may play an important role in the synthesis of cytosolic argininosuccinate.
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Pardo, Beatriz, Tiago B. Rodrigues, Laura Contreras, Miguel Garzón, Irene Llorente-Folch, Keiko Kobayashi, Takeyori Saheki, Sebastian Cerdan, and Jorgina Satrústegui. "Brain Glutamine Synthesis Requires Neuronal-Born Aspartate as Amino Donor for Glial Glutamate Formation." Journal of Cerebral Blood Flow & Metabolism 31, no. 1 (August 25, 2010): 90–101. http://dx.doi.org/10.1038/jcbfm.2010.146.

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The glutamate–glutamine cycle faces a drain of glutamate by oxidation, which is balanced by the anaplerotic synthesis of glutamate and glutamine in astrocytes. De novo synthesis of glutamate by astrocytes requires an amino group whose origin is unknown. The deficiency in Aralar/ AGC1, the main mitochondrial carrier for aspartate–glutamate expressed in brain, results in a drastic fall in brain glutamine production but a modest decrease in brain glutamate levels, which is not due to decreases in neuronal or synaptosomal glutamate content. In vivo13C nuclear magnetic resonance labeling with 13C2acetate or (1-13C) glucose showed that the drop in brain glutamine is due to a failure in glial glutamate synthesis. Aralar deficiency induces a decrease in aspartate content, an increase in lactate production, and lactate-to-pyruvate ratio in cultured neurons but not in cultured astrocytes, indicating that Aralar is only functional in neurons. We find that aspartate, but not other amino acids, increases glutamate synthesis in both control and aralar-deficient astrocytes, mainly by serving as amino donor. These findings suggest the existence of a neuron-to-astrocyte aspartate transcellular pathway required for astrocyte glutamate synthesis and subsequent glutamine formation. This pathway may provide a mechanism to transfer neuronal-born redox equivalents to mitochondria in astrocytes.
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Hertz, Leif. "Brain Glutamine Synthesis Requires Neuronal Aspartate: A Commentary." Journal of Cerebral Blood Flow & Metabolism 31, no. 1 (November 10, 2010): 384–87. http://dx.doi.org/10.1038/jcbfm.2010.199.

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Inspired by the paper, ‘Brain glutamine synthesis requires neuronal-born aspartate as amino donor for glial glutamate formation’ by Pardo et al, a modified model of oxidation–reduction, transamination, and mitochondrial carrier reactions involved in aspartate-dependent astrocytic glutamine synthesis and oxidation is proposed. The alternative model retains the need for cytosolic aspartate for transamination of α-ketoglutarate, but the ‘missing’ aspartate molecule is generated within astrocytes during subsequent glutamate oxidation. Oxaloacetate formed during glutamate formation is used during glutamate degradation, and all transmitochondrial reactions, oxidations–reductions, and cytosolic and mitochondrial transaminations are stoichiometrically balanced. The model is consistent with experimental observations made by Pardo et al.
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Khalish, Mutiara, and Lathifah Yasmine Wulandari. "The Vitamin C Berpengaruh dalam Memperbaiki Kerusakan Hepar Akibat Pemberian Monosodium Glutamat." Jurnal Penelitian Perawat Profesional 2, no. 2 (March 14, 2020): 125–30. http://dx.doi.org/10.37287/jppp.v2i2.67.

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Konsumsi monosodium glutamat dalam jumlah berlebih dapat menyebabkan dampak berkaitan dengan kerusakan hepar yang ditandai adanya peningkatan kadar enzim aspartate transaminase dan alanine transaminase. Vitamin c berperan menjaga sistem imunitas tubuh dan mempercepat proses penyembuhan kerusakan hepar. Tujuan penulisan artikel ini adalah untuk mengetahui manfaat vitamin c sebagai upaya dalam memperbaiki kerusakan hepar akibat monosodium glutamat. Metode yang digunakan dalam artikel ini adalah penelusuran artikel melalui database Google Scholar, NCBI dan Elsevier. Tahun penerbitan pustaka adalah dari tahun 2010 hingga 2019 dengan 17 sumber pustaka. Hasil dari literatur review ini menunjukan bahwa vitamin c dapat mengurangi kerusakan hepar akibat monosodium glutamat dengan adanya penurunan kadar enzim aspartate transaminase dan alanine transaminase. Vitamin c dapat digunakan untuk melawan efek radikal bebas dari monosodium glutamat karena aktifitasnya sebagai antioksidan. Vitamin c berpengaruh dalam memperbaiki kerusakan hepar akibat pemberian monosodium glutamat. Kata kunci: aspartate transaminase, alanine transaminase, monosodium glutamat, vitamin c VITAMIN C AFFECT IN IMPROVING HEPAR DAMAGE CAUSED BY ADMINISTRATION OF MONOSODIUM GLUTAMATE ABSTRACT Excessive consumption of monosodium glutamate can cause effects related to liver damage which is marked by an increase in levels of the enzymes aspartate transaminase and alanine transaminase. Vitamin c plays a role in maintaining the body's immune system and accelerating the healing process of liver damage. The purpose of writing this article is to determine the benefits of vitamin c as an effort to repair liver damage due to monosodium glutamate. The method used in this article is article searching through Google Scholar, NCBI and Elsevier databases. The year of library publication is from 2010 to 2019 with 17 library sources. The results of this review literature show that vitamin c can reduce liver damage due to monosodium glutamate by decreasing levels of the enzymes aspartate transaminase and alanine transaminase. Vitamin C can be used to fight the effects of free radicals from monosodium glutamate because of its activity as an antioxidant. Vitamin C has an effect on repairing liver damage due to monosodium glutamate. Keywords: aspartate transaminase, alanine transaminase, monosodium glutamate, vitamin c
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Martin, G., C. Michoudet, N. Vincent, and G. Baverel. "Release and fixation of CO2 by guinea-pig kidney tubules metabolizing aspartate." Biochemical Journal 284, no. 3 (June 15, 1992): 697–703. http://dx.doi.org/10.1042/bj2840697.

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1. The metabolism of L-[U-14C]aspartate, L-[1-14C]aspartate and L-[4-14C]aspartate was studied in isolated guinea-pig kidney tubules. 2. Oxidation of C-1 plus that of C-4 of aspartate accounted for 90-92% of the CO2 released from aspartate, whereas oxidation of the inner carbon atoms of aspartate (which occurs beyond the 2-oxoglutarate dehydrogenase step) represented only 8-10% of aspartate carbon oxidation. 3. The formation of [1-14C]glutamine and [1-14C]glutamate from [1-14C]aspartate and [4-14C]aspartate indicated that about one-third of the oxaloacetate synthesized from aspartate underwent randomization at the level of fumarate. 4. With [U-14C]aspartate as substrate, the percentage of the C-1 of glutamate and glutamine found radiolabelled after 60 min of incubation was 92.7% and 47.5% in the absence and the presence of bicarbonate respectively. 5. That CO2 fixation occurred at high rates in the presence of bicarbonate was demonstrated by incubating tubules with aspartate plus [14C]bicarbonate; under this condition, the label fixed was found in C-1 of glutamate, glutamine and aspartate, as well as in C-4 of aspartate, demonstrating not only randomization of aspartate carbon but also aspartate resynthesis secondary to oxaloacetate cycling via phosphoenolpyruvate carboxykinase, pyruvate kinase and pyruvate carboxylase. 6. The importance of CO2 fixation in glutamine synthesis from aspartate is discussed in relation to the possible role of the guinea-pig kidney in systemic acid-base regulation in vivo.
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Nianhui, Zhang, and P. Ottersen Ole. "In Search of the Identity of the Cerebellar Climbing Fiber Transmitter: Immunocytochemical Studies in Rats." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 20, S3 (May 1993): S36—S42. http://dx.doi.org/10.1017/s0317167100048514.

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ABSTRACT:Quantitative immunogold cytochemistry at the electron microscopic level was used to assess the endogenous contents of glutamate, aspartate, homocysteic acid, and glutamine (a precursor of glutamate) in the cerebellar climbing fiber terminals. Of the three excitatory amino acids, only glutamate appeared to be enriched in these terminals. The climbing fiber terminals also displayed immunoreactivity for glutamine. The level of aspartate immunoreactivity was far higher in the nerve cell bodies in the inferior olive than in their terminals in the cerebellar cortex. Homocysteic acid immunolabelling was concentrated in glial cells including the Golgi epithelial cells in the Purkinje cell layer. Our immunocytochemical data indicate that glutamate is a more likely climbing fiber transmitter than aspartate and homocysteic acid.
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Osbakken, M., D. N. Zhang, D. Nelson, and M. Erecinska. "Effect of cyclocreatine feeding on levels of amino acids in rat hearts before and after an ischemic episode." American Journal of Physiology-Heart and Circulatory Physiology 261, no. 6 (December 1, 1991): H1919—H1926. http://dx.doi.org/10.1152/ajpheart.1991.261.6.h1919.

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Feeding Sprague-Dawley rats for 3 wk a diet containing 1% by weight of cyclocreatine increased the reservoir of the high-energy phosphate compounds but also caused alterations in the levels of the two key amino acids, aspartate and glutamate. Both were decreased by approximately 50% in the presence of an unaltered content of glutamine. In vitro exposure of these hearts to sequential perfusion, global ischemia, and reperfusion in the absence of added amino acids resulted in changes in aspartate, glutamate, and glutamine that were different from those in hearts from control rats. In the cyclocreatine-fed group, aspartate concentration ([aspartate]) and [glutamate] fell after global ischemia, whereas [glutamine] was unaltered. [Glutamine] decreased, however, in the reperfusion period. In control hearts, the predominant effect was a steady decline in glutamine, which was accompanied by either less than 10% (after global ischemia) or 30-50% fall (after reperfusion) in [aspartate] and [glutamate]. The concentration of tissue Pi was smaller in hearts from cyclocreatine-fed rats and appeared to increase more slowly during ischemia. In the presence of rotenone and aminooxyacetate, heart homogenates catalyzed production of glutamate from glutamine, which was markedly stimulated by Pi and inhibited by H+. It is postulated that 1) phosphate-activated glutaminase is an important enzyme that determines cardiac [glutamate], 2) lower [phosphate] in hearts from rats fed cyclocreatine is responsible for the apparently lesser activity of glutaminase, 3) breakdown of the high-energy phosphate compounds and consequent rise in Pi activates glutaminase, and 4) slow breakdown of glutamine during global ischemia is a result of inhibition of glutaminase by H+.
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Baverel, G., G. Martin, and C. Michoudet. "Glutamine synthesis from aspartate in guinea-pig renal cortex." Biochemical Journal 268, no. 2 (June 1, 1990): 437–42. http://dx.doi.org/10.1042/bj2680437.

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1. Glutamine was found to be the main carbon and nitrogen product of the metabolism of aspartate in isolated guinea-pig kidney-cortex tubules. Glutamate, ammonia and alanine were only minor products. 2. Carbon-balance calculations and the release of 14CO2 from [U-14C]aspartate indicate that oxidation of the aspartate carbon skeleton occurred. 3. A pathway involving aspartate aminotransferase, glutamate dehydrogenase, glutamine synthetase, phosphoenolpyruvate carboxykinase, pyruvate kinase, pyruvate dehydrogenase and enzymes of the tricarboxylic acid cycle is proposed for the conversion of aspartate into glutamine. 4. Evidence for this pathway was obtained by: (i) inhibiting aspartate removal by amino-oxyacetate, an inhibitor of transaminases, (ii) the use of methionine sulphoximine, an inhibitor of glutamine synthetase, which induced a large increase in ammonia release from aspartate, (iii) the use of quinolinate, an inhibitor of phosphoenolpyruvate carboxykinase, which inhibited glutamine synthesis from aspartate, (iv) the use of alpha-cyano-4-hydroxycinnamate, an inhibitor of the mitochondrial transport of pyruvate, which caused an accumulation of pyruvate from aspartate, and (v) the use of fluoroacetate, an inhibitor of aconitase, which inhibited glutamine synthesis with concomitant accumulation of citrate from aspartate.
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Gundersen, Vidar, Frode Fonnum, Ole Petter Ottersen, and Jon Storm-Mathisen. "Redistribution of Neuroactive Amino Acids in Hippocampus and Striatum during Hypoglycemia: A Quantitative Immunogold Study." Journal of Cerebral Blood Flow & Metabolism 21, no. 1 (January 2001): 41–51. http://dx.doi.org/10.1097/00004647-200101000-00006.

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Postembedding immunocytochemistry was used to localize aspartate, glutamate, gamma-aminobutyric acid (GABA), and glutamine in hippocampus and striatum during normo- and hypoglycemia in rat. In both brain regions, hypoglycemia caused aspartatelike immunoreactivity to increase. In hippocampus, this increase was evident particularly in the terminals of known excitatory afferents—in GABA-ergic neurons and myelinated axons. Aspartate was enriched along with glutamate in nerve terminals forming asymmetric synapses on spines and with GABA in terminals forming symmetric synapses on granule and pyramidal cell bodies. In both types of terminal, aspartate was associated with clusters of synaptic vesicles. Glutamate and glutamine immunolabeling were markedly reduced in all tissue elements in both brain regions, but less in the terminals than in the dendrosomatic compartments of excitatory neurons. In glial cells, glutamine labeling showed only slight attenuation. The level of GABA immunolabeling did not change significantly during hypoglycemia. The results support the view that glutamate and glutamine are used as energy substrates in hypoglycemia. Under these conditions both excitatory and inhibitory terminals are enriched with aspartate, which may be released from these nerve endings and thus contribute to the pattern of neuronal death characteristic of hypoglycemia.
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Lietz, T., K. Winiarska, and J. Bryła. "Ketone bodies activate gluconeogenesis in isolated rabbit renal cortical tubules incubated in the presence of amino acids and glycerol." Acta Biochimica Polonica 44, no. 2 (June 30, 1997): 323–31. http://dx.doi.org/10.18388/abp.1997_4428.

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In isolated rabbit renal kidney-cortex tubules 2 mM glycerol, which is a poor gluconeogenic substrate, does not induce glucose formation in the presence of alanine, while it activates gluconeogenesis on substitution of alanine by aspartate, glutamate or proline. The addition of either 5 mM 3-hydroxybutyrate or 5 mM acetoacetate to renal tubules incubated with alanine + glycerol causes a marked induction of glucose production associated with inhibition of glutamine synthesis. In contrast, the rate of the latter process is not altered by ketones in the presence of glycerol and either aspartate, glutamine or proline despite the stimulation of glucose formation. Acceleration of gluconeogenesis by ketone bodies in the presence of amino acids and glycerol is probably due to (i) stimulation of pyruvate carboxylase activity, (ii) activation of malate-aspartate shuttle as concluded from elevated intracellular levels of malate, aspartate and glutamate, as well as (iii) diminished supply of ammonium for glutamine synthesis from alanine resulting from a decrease in glutamate dehydrogenase activity.
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Dissertations / Theses on the topic "Glutamate and aspartate"

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Fisch, Florian A. "Catalytic plasticity of the aspartate/glutamate racemase superfamily." Thesis, University of York, 2009. http://etheses.whiterose.ac.uk/799/.

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The bacterial and archaeal Asp/Glu racemase enzyme superfamily contains a variety of catalytic functions that have great potential for use in industrial biocatalysis. Members of this superfamily include aspartate racemases (AspRs), glutamate racemases (GluRs), hydantoin racemases (HydRs), arylmalonate decarboxylases (AMDs) and maleate cis-trans isomerases (MIs). Despite their catalytic diversity, all characterised members share the same protein fold, catalytic cysteine residues and reaction intermediate. Attempts to exploit this evolutionary flexibility for new processes have had limited success so far, showing that the employed mechanisms are not yet fully understood. For example, the well-characterised Bordetella bronchiseptica AMD (BbAMD) enantiospecifically decarboxylates a range of arylmalonates was but is not able to decarboxylate alkylmalonates despite considerable efforts made by site directed mutagenesis. In this work an investigation of the sequence diversity of the superfamily was undertaken and a range of BbAMD sequence homologues was tested for both aryl- and alkylmalonate decarboxylation (Chapter 3). However, none of the homologues exhibited decarboxylation activity. Targeted mutation of active site residues in an attempt to introduce decarboxylase activity was also unsuccessful. In an alternative approach to identify new alkylmalonate decarboxylating enzymes, a range of bacterial strains capable of processing alkylmalonates was isolated using selective enrichment from soil samples (Appendix D). The only characterised superfamily enzymes without a described three dimensional protein structure are MIs. In order to illuminate the distinct mechanism of MIs, the activity of the superfamily member Nocardia farcinica MI (NfMI) was characterised (Chapter 4) and its structure was determined by X-ray crystallography (Chapter 5). A potent inhibitor and substrate analogue bromomaleate was found. Mutagenesis of the active site cysteine dyad confirmed its catalytic role and Cys76 was found to be more important than Cys194. The data support a mechanism initiated by nucleophilic attack by Cys76 on the double bond of maleate. Although alternative mechanisms cannot be excluded at present, these findings indicate that the mechanistic chemistry in the superfamily is more adaptable than previously thought.
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Crawford, Martin. "Neurotransmitter interactions within the rat neostratum." Thesis, University of Southampton, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.280360.

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Yassin, Maged M. I. "N-methyl-D-aspartate, anoxia and glutamate antagonists in mammalian brain." Thesis, Queen's University Belfast, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.241524.

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Thangaratnarajah, Chancievan. "The structural and functional characterisation of the mitochondrial aspartate-glutamate carriers." Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708769.

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Tofighy, Azita. "N-methyl-d-aspartate receptor desensitisation and anoxia in rat olfactory cortex." Thesis, Queen's University Belfast, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.361309.

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Dean, Jonathan Lewis. "The roles of aspartate and arginine in the active site of glutamate dehydrogenase." Thesis, University of Sheffield, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388695.

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Williams, Helen. "The transport and cardioprotective action of glutamate and aspartate in isolated ventricular myocytes." Thesis, University of Bristol, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299276.

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

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Hobbs, Catherine M. "The functional expression of N-methyl-D-aspartate glutamate-type receptors by megakaryocytes and platelets." Thesis, University of Bath, 2010. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.527791.

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This study investigated the role of NMDARs in the differentiation of MEG-01 cells and in the activation of human platelets. This investigation demonstrated that the NR1, NR2D and NR3 subunit proteins are expressed in human platelets, with the NR1 subunit also expressed in MEG-01 cells. The NR2A subunit protein was not detectable in either MEG-01 cells or human platelets. PMA-induced differentiation of MEG-01 cells did not appear to stimulate changes in expression of any of the subunit proteins tested. Using assays to measure the changes in [Ca2+]i and ATP secretion, it was determined that donors could be separated into those who responded to the agonists applied and those who did not; responses also decreased over time in both assays. Human platelets from responding donors demonstrate an increase in [Ca2+]i in response to extracellular glutamate, and that increases in ATP secretion are detected at a 10-fold lower concentration. The same is also true with extracellular glycine. Increases in [Ca2+]i were elicited on the addition of extracellular NMDA; extracellular D-serine had no effect. NMDAR inhibitors, MK-801 and D-AP5, inhibited ATP secretion evoked by either glutamate alone or in combination with glycine. D-serine inhibited responses elicited by extracellular glycine. NMDARs play a role in MK differentiation, with the adhesion of MEG-01 cells cultured on a fibrinogen-surface and differentiated with PMA reduced by both inhibitors. PMA-treated MEG-01 cells increased both in size and irregularity, with the addition of NMDAR-specific inhibitors having no effect. S-nitrosylation also inhibits activation of NMDAR, and a new molecule has been developed which can detect S-nitrosylated proteins through a single step process in live cells. Overall, this study has shown that both human platelets and MEG-01 cells express NMDAR subunits, which have been demonstrated to form functional receptors in human platelets.
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Bright, Nieka L. "Glutamate Receptor, Ionotropic N-methyl-D-aspartate 2B Polymorphisms and Concussive Recovery in Athletes." Diss., Temple University Libraries, 2013. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/216565.

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Kinesiology
Ph.D.
Athletes vary in their ability to recover from concussions. Following a concussion, a pathophysiological cascade of events transpires, rendering symptoms. One such event, the indiscriminate release of the excitatory neurotransmitter glutamate, may result in hyperactivation of glutamate receptors (e.g., N-methyl-D-aspartate receptors [NMDARs]) and self-propagate a state of neurotoxicity that may be enhanced via the concomitant release of Ca2+, particularly through NMDARs containing the NR2B subunit. Genetic variation in regulatory regions of the glutamate receptor, ionotropic N-methyl-D-aspartate 2B (GRIN2B) gene, which codes for the NR2B subunit, may play a role in varied recovery among concussed athletes. Indeed, the rs1019385 promoter single nucleotide polymorphism (SNP) has been shown to alter transcription in dominant versus recessive allele carriers such that expression of the T allele results in increased upregulation of the GRIN2B gene. Therefore, the primary purpose of this study was to determine the association of this GRIN2B SNP and concussive recovery; a second GRIN2B SNP (rs890), in the 3'untranslated region, was also explored. A secondary purpose was to examine SNP associations with initial evaluation concussion severity scores. A triple-blind, between-subjects, genetic association design was utilized. The independent variable was genotype for both GRIN2B SNPs (rs1019385, rs890). The primary dependent variable, concussive recovery, was defined as the number of days from the time of injury until full return-to-play (RTP) clearance was granted by a university concussion center's physician; recovery was categorized as either normal (≤ 20 days) or prolonged (> 20 days). The secondary dependent variables were initial evaluation concussion severity scores and consisted of: (a) vestibulo-ocular reflex (VOR) result, (b) Balance Error Scoring System (BESS) sum, and (c) Immediate Postconcussion Assessment and Cognitive Testing (ImPACT) composite scores. Fifty-three, mostly White (69.7%), male (75.0%) concussed athletes (18.96 ± 6.31 years of age) participated in the study; two participants were excluded due to inconclusive genetic results. Participants were evaluated at a university concussion center per standardized concussion assessment battery, using the aforementioned severity indicators, and provided saliva samples for genotyping experiments. Follow-up visits were performed, as needed, until participants were asymptomatic and cleared for full RTP. No significant associations were demonstrated for the codominant (p = .35, p = .70), dominant (p = .39, p = 1.00) or recessive (p = .72, p = .51) genetic models for the rs1019385 and rs890 SNPs (respectively). Similarly, there were no significant differences in any initial evaluation severity scores between genotype for any genetic model. This exploratory study investigated the association between two GRIN2B SNPs and varied concussive recovery among athletes. Although no statistical and minimal clinical significance was demonstrated, future investigations should incorporate a larger sample and next-generation sequencing to investigate the 21,000 to 25,000 genes and their variations across the human genome as complex disorders (e.g., concussions) likely involve a multitude of genetic variations (and their interactions), many with small effects. Further elucidation of genetic factors involved in concussive recovery could equip clinicians with superior counseling methods and treatment options for athletes at-risk for prolonged recovery.
Temple University--Theses
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Books on the topic "Glutamate and aspartate"

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Brown, Jennifer Ann. Effects of kainic and domoic acids on the release of glutamate and aspartate from rat brain synaptosomes. Charlottetown: University of Prince Edward Island, 1992.

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Brown, Jennifer Ann. Effects of kainic and domoic acids on the release of glutamate and aspartate from the rat brain synsptosomes. Ottawa: National Library, 1992.

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Sinasac, David Steven. Cloning and characterization of citrin: The aspartate/glutamate carrier mutated in adult-onset type II citrullinemia. 2003.

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Black, Sheila. The original description of central sensitization. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0040.

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The landmark study discussed in this chapter is ‘The contribution of excitatory amino acids to central sensitization and persistent nociception after formalin-induced tissue injury’, published by Coderre and Melzack in 1992. Previous studies in this field implicate a contribution of excitatory amino acids (EAAs), specifically l-glutamate and l-aspartate, to injury-induced sensitization of nociceptive responses in the dorsal horn of the spinal cord. Repetitive stimulation of primary afferent fibres demonstrated that l-glutamate and NMDA can produce ‘wind-up’ of neuronal dorsal horn activity, and this is blocked by application of NMDA antagonists. This study uses the formalin test as a behavioural model to investigate the mechanisms underlying central sensitization and the role of EAAs, NMDA, their receptors, and their antagonists in this process.
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Henter, Ioline D., and Rodrigo Machado-Vieira. Novel therapeutic targets for bipolar disorder. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198748625.003.0030.

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The long-term course of bipolar disorder (BD) comprises recurrent depressive episodes and persistent residual symptoms for which standard therapeutic options are scarce and often ineffective. Glutamate is the major excitatory neurotransmitter in the central nervous system, and glutamate and its cognate receptors have consistently been implicated in the pathophysiology of mood disorders and in the development of novel therapeutics for these disorders. Since the rapid and robust antidepressant effects of the N-methyl-D-aspartate (NMDA) antagonist ketamine were first observed in 2000, other NMDA receptor antagonists have been studied in major depressive disorder (MDD) and BD. This chapter reviews the clinical evidence supporting the use of novel glutamate receptor modulators for treating BD—particularly bipolar depression. We also discuss other promising, non-glutamatergic targets for potential rapid antidepressant effects in mood disorders, including the cholinergic system, the melatonergic system, the glucocorticoid system, the arachidonic acid (AA) cascade, and oxidative stress and bioenergetics.
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Book chapters on the topic "Glutamate and aspartate"

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Kobayashi, Keiko, and Takeyori Saheki. "Aspartate glutamate carrier (citrin) deficiency." In Membrane Transporter Diseases, 147–60. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9023-5_10.

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Schomburg, Dietmar, Margit Salzmann, and Dörte Stephan. "D-Glutamate(D-aspartate) oxidase." In Enzyme Handbook, 875–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-58051-2_179.

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McGeer, Patrick L., John C. Eccles, and Edith G. McGeer. "Putative Excitatory Neurons: Glutamate and Aspartate." In Molecular Neurobiology of the Mammalian Brain, 175–96. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4615-7497-2_6.

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Rolf, L. H., Th Klauke, E. W. Fünfgeld, and G. G. Brune. "Aspartate, glutamate, and glutamine in platelets of patients with Parkinson’s disease." In Key Topics in Brain Research, 221–27. Vienna: Springer Vienna, 1989. http://dx.doi.org/10.1007/978-3-7091-8994-8_26.

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Gopinath, Shankar P., A. B. Valadka, J. C. Goodman, and C. S. Robertson. "Extracellular Glutamate and Aspartate in Head Injured Patients." In Brain Edema XI, 437–38. Vienna: Springer Vienna, 2000. http://dx.doi.org/10.1007/978-3-7091-6346-7_90.

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Drummond, John C. "Are Glutamate/Aspartate Antagonists Protective in Cerebral Ischemia?" In Advances in Brain Resuscitation, 45–57. Tokyo: Springer Japan, 1991. http://dx.doi.org/10.1007/978-4-431-68538-8_3.

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Skolnick, Phil, Piotr Popik, and Ramon Trullas. "N-Methyl-d-Aspartate (NMDA) Antagonists for the Treatment of Depression." In Glutamate-based Therapies for Psychiatric Disorders, 1–20. Basel: Birkhäuser Basel, 2010. http://dx.doi.org/10.1007/978-3-0346-0241-9_1.

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Bleich, Stefan, and Johannes Kornhuber. "Glutamate and Schizophrenia and the N-Methyl-d-Aspartate Receptor Hypofunction Hypothesis." In Dopamine and Glutamate in Psychiatric Disorders, 169–79. Totowa, NJ: Humana Press, 2005. http://dx.doi.org/10.1007/978-1-59259-852-6_7.

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Shank, R. P., and G. Le M. Campbell. "Metabolic Precursors of the Transmitter Pools of Glutamate and Aspartate." In Excitatory Amino Acids, 47–56. London: Palgrave Macmillan UK, 1986. http://dx.doi.org/10.1007/978-1-349-08479-1_3.

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Giuffrida, Rosario, and Aldo Rustioni. "Glutamate and aspartate in corticofugal neurons: A combined immunocytochemical and tracing study." In Amino Acids, 488–96. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-011-2262-7_57.

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Conference papers on the topic "Glutamate and aspartate"

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Gagné, Jean-Philippe, Florence Roux-Dalvai, Daniel Defoy, Arnaud Droit, Hendzel J. Michael, and Guy G. Poirier. "Abstract A42: Identification of glutamate and aspartate ADP-ribosylation sites onto histones by mass mass spectrometry." In Abstracts: AACR Special Conference on DNA Repair: Tumor Development and Therapeutic Response; November 2-5, 2016; Montreal, QC, Canada. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1557-3125.dnarepair16-a42.

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Golovynska, Iuliia, Tatiana V. Beregova, Tatiana M. Falalyeyeva, Sergii Golovynskyi, Junle Qu, and Tymish Y. Ohulchanskyy. "Combining optical imaging and pharmacological methods to localize N-methyl-D-aspartate glutamate receptors in a stomach wall." In International Conference on Photonics and Imaging in Biology and Medicine. Washington, D.C.: OSA, 2017. http://dx.doi.org/10.1364/pibm.2017.w3a.107.

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Kizilbash, Sani Haider, Danielle M. Burgenske, Samuel McBrayer, Sandhya Devarajan, Shiv K. Gupta, Taro Hitosugi, Lihong He, et al. "Abstract 3870: The addition of CB-839 to temozolomide significantly reduces glioma aspartate and glutamate in an IDH mutated patient derived glioma xenograft model." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3870.

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Kizilbash, Sani Haider, Danielle M. Burgenske, Samuel McBrayer, Sandhya Devarajan, Shiv K. Gupta, Taro Hitosugi, Lihong He, et al. "Abstract 3870: The addition of CB-839 to temozolomide significantly reduces glioma aspartate and glutamate in an IDH mutated patient derived glioma xenograft model." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-3870.

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