Artículos de revistas: "Cerebrospinal fluid Glutamine synthetase"

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Tumani, Hayrettin, GuoQiu Shen, James B. Peter y Wolfgang Brück. "Glutamine Synthetase in Cerebrospinal Fluid, Serum, and Brain". Archives of Neurology 56, n.º 10 (1 de octubre de 1999): 1241. http://dx.doi.org/10.1001/archneur.56.10.1241.

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Timmer, Nienke M., Megan K. Herbert, Jurgen A. H. R. Claassen, H. Bea Kuiperij y Marcel M. Verbeek. "Total glutamine synthetase levels in cerebrospinal fluid of Alzheimer's disease patients are unchanged". Neurobiology of Aging 36, n.º 3 (marzo de 2015): 1271–73. http://dx.doi.org/10.1016/j.neurobiolaging.2014.12.010.

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Gunnersen, D. y B. Haley. "Detection of glutamine synthetase in the cerebrospinal fluid of Alzheimer diseased patients: a potential diagnostic biochemical marker." Proceedings of the National Academy of Sciences 89, n.º 24 (15 de diciembre de 1992): 11949–53. http://dx.doi.org/10.1073/pnas.89.24.11949.

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Herbert, Megan K., H. Bea Kuiperij y Marcel M. Verbeek. "Optimisation of the quantification of glutamine synthetase and myelin basic protein in cerebrospinal fluid by a combined acidification and neutralisation protocol". Journal of Immunological Methods 381, n.º 1-2 (julio de 2012): 1–8. http://dx.doi.org/10.1016/j.jim.2012.04.001.

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Tumani, Hayrettin, Guo Qui Shen y James B. Peter. "Purification and immunocharacterization of human brain glutamine synthetase and its detection in cerebrospinal fluid and serum by a sandwich enzyme immunoassay". Journal of Immunological Methods 188, n.º 1 (diciembre de 1995): 155–63. http://dx.doi.org/10.1016/0022-1759(95)00215-4.

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Jaeken, J., P. Casaer y L. Corbeel. "Valproate increases cerebrospinal fluid glutamine levels". European Journal of Pediatrics 146, n.º 1 (enero de 1987): 91. http://dx.doi.org/10.1007/bf00647300.

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Levine, Joseph, Kanagasabai Panchalingam, Avraham Rapoport, Samuel Gershon, Richard J. McClure y Jay W. Pettegrew. "Increased cerebrospinal fluid glutamine levels in depressed patients". Biological Psychiatry 47, n.º 7 (abril de 2000): 586–93. http://dx.doi.org/10.1016/s0006-3223(99)00284-x.

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Rothrock, JF, KR Mar, TL Yaksh, A. Golbeck y AC Moore. "Cerebrospinal Fluid Analyses in Migraine Patients and Controls". Cephalalgia 15, n.º 6 (diciembre de 1995): 489–93. http://dx.doi.org/10.1046/j.1468-2982.1995.1506489.x.

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To investigate the role of central neurotransmitters in the pathogenesis of migraine, we measured cerebrospinal fluid (CSF) levels of certain amino acids (glycine, taurine, glutamine) and metabolites of biogenic amines (5-hydroxyindoleacetic acid and homovanillic acid) in 38 migraine patients and compared them with the levels from 10 headache-free controls. The levels of taurine, glycine and glutamine were significantly higher in the migraine patients (p < 0.0001 for taurine and glycine; p < 0.0009 for glutamine); there were no significant differences among the three migraine subgroups (infrequent migraine, frequent migraine and transformed migraine). In seven patients subsequently treated with divalproex sodium, CSF taurine levels decreased significantly from pretreatment baseline values. These data support the concept that migraine is at least in part a disorder of central neurotransmission.

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ANDERSEN, ERIK ARTHUR y DITLEF BUCHER. "Cerebrospinal Fluid Glutamine in Intracranial Hemorrhage in the Newborn". Acta Paediatrica 75, n.º 6 (noviembre de 1986): 899–904. http://dx.doi.org/10.1111/j.1651-2227.1986.tb10314.x.

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Aasly, J., M. Gårseth, U. Sonnewald, J. A. Zwart, L. R. White y G. Unsgård. "Cerebrospinal fluid lactate and glutamine are reduced in multiple sclerosis". Acta Neurologica Scandinavica 95, n.º 1 (enero de 1997): 9–12. http://dx.doi.org/10.1111/j.1600-0404.1997.tb00060.x.

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Pogorelova, T. N., V. O. Gunko y V. A. Linde. "Imbalance of system of glutamin – glutamic acid in the placenta and amniotic fluid at placental insufficiency". Biomeditsinskaya Khimiya 60, n.º 5 (2014): 596–601. http://dx.doi.org/10.18097/pbmc20146005596.

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Metabolism of glutamine and glutamic acid has been investigated in the placenta and amniotic fluid under conditions of placental insufficiency. The development of placental insufficiency is characterized by the increased content of glutamic acid and a decrease of glutamine in both placenta and amniotic fluid. These changes changes were accompanied by changes in the activity of enzymes involved in the metabolism of these amino acids. There was a decrease in glutamate dehydrogenase activity and an increase in glutaminase activity with the simultaneous decrease of glutamine synthetase activity. The compensatory decrease in the activity of glutamine keto acid aminotransferase did not prevent a decrease in the glutamine level. The impairments in the system glutamic acid-glutamine were more pronounced during the development of premature labor.

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Xiang, Jianming, Steven R. Ennis, Galaleldin E. Abdelkarim, Mutsuo Fujisawa, Nobuyuki Kawai y Richard F. Keep. "Glutamine transport at the blood–brain and blood–cerebrospinal fluid barriers". Neurochemistry International 43, n.º 4-5 (septiembre de 2003): 279–88. http://dx.doi.org/10.1016/s0197-0186(03)00013-5.

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El-Yazigi, Adnan y Ossama Al-Mefty. "Decreased Cerebrospinal Fluid Glutamine Levels in Patients with Benign Brain Tumors". Journal of Neurochemistry 45, n.º 3 (septiembre de 1985): 815–18. http://dx.doi.org/10.1111/j.1471-4159.1985.tb04066.x.

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Coplan, Jeremy D., Nishant K. Gupta, Sarah K. Flynn, Wade J. Reiner, David Gaita, Sasha L. Fulton, Anna V. Rozenboym, Jean E. Tang, Thomas B. Cooper y J. John Mann. "Maternal Cerebrospinal Fluid Glutamate in Response to Variable Foraging Demand: Relationship to Cerebrospinal Fluid Serotonin Metabolites in Grown Offspring". Chronic Stress 2 (enero de 2018): 247054701878562. http://dx.doi.org/10.1177/2470547018785625.

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Background Maternal response to allostatic overload during infant rearing may alter neurobiological measures in grown offspring, potentially increasing susceptibility to mood and anxiety disorders. We examined maternal cerebrospinal fluid (CSF) glutamate response during exposure to variable foraging demand (VFD), a bonnet macaque model of allostatic overload, testing whether activation relative to baseline predicted concomitant CSF elevations of the stress neuropeptide, corticotropin-releasing factor. We investigated whether VFD-induced activation of maternal CSF glutamate affects maternal–infant attachment patterns and offspring CSF 5-hydroxyindoleacetic acid concentrations. Methods Mother–infant dyads were exposed to the “VFD stressor,” a paradigm in which mothers experience 16 weeks of foraging uncertainty while rearing their infant offspring. Through staggering the infant age of VFD onset, both a cross-sectional design and a longitudinal design were used. Maternal CSF glutamate and glutamine concentrations post-VFD exposure were cross-sectionally compared to maternal VFD naive controls. Proportional change in concentrations of maternal glutamate (and glutamine), a longitudinal measure, was evaluated in relation to VFD-induced elevations of CSF corticotropin-releasing factor. The former measure was related to maternal–infant proximity scores obtained during the final phases of VFD exposure. Maternal glutamatergic response to VFD exposure was used as a predictor variable for young adolescent offspring CSF metabolites of serotonin, dopamine, and norepinephrine. Results Following VFD exposure, maternal CSF glutamate concentrations correlated positively with maternal CSF CRF concentrations. Activation relative to baseline of maternal CSF glutamate concentrations following VFD exposure correlated directly with a) increased maternal-infant proximity during the final phases of VFD and b) offspring CSF concentrations of monoamine metabolites including 5-hydroxyindoleacetic acid, which was elevated relative to controls. Conclusions Activation of maternal CSF glutamate in response to VFD-induced allostasis is directly associated with elevations of maternal CSF corticotropin-releasing factor. Maternal CSF glutamate alterations induced by VFD potentially compromise serotonin neurotransmission in grown offspring, conceivably modeling human vulnerability to treatment-resistant mood and anxiety disorders.

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Hiraoka, Atsushi, Isao Miura, Itaru Tominaga y Munekazu Hattori. "Capillary-isotachophoretic determination of glutamine in cerebrospinal fluid of various neurological disorders". Clinical Biochemistry 22, n.º 4 (agosto de 1989): 293–96. http://dx.doi.org/10.1016/s0009-9120(89)80020-7.

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Dolgodilina, Elena, Stefan Imobersteg, Endre Laczko, Tobias Welt, Francois Verrey y Victoria Makrides. "Brain interstitial fluid glutamine homeostasis is controlled by blood–brain barrier SLC7A5/LAT1 amino acid transporter". Journal of Cerebral Blood Flow & Metabolism 36, n.º 11 (22 de julio de 2016): 1929–41. http://dx.doi.org/10.1177/0271678x15609331.

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L-glutamine (Gln) is the most abundant amino acid in plasma and cerebrospinal fluid and a precursor for the main central nervous system excitatory (L-glutamate) and inhibitory (γ-aminobutyric acid (GABA)) neurotransmitters. Concentrations of Gln and 13 other brain interstitial fluid amino acids were measured in awake, freely moving mice by hippocampal microdialysis using an extrapolation to zero flow rate method. Interstitial fluid levels for all amino acids including Gln were ∼5–10 times lower than in cerebrospinal fluid. Although the large increase in plasma Gln by intraperitoneal (IP) injection of 15N2-labeled Gln (hGln) did not increase total interstitial fluid Gln, low levels of hGln were detected in microdialysis samples. Competitive inhibition of system A (SLC38A1&2; SNAT1&2) or system L (SLC7A5&8; LAT1&2) transporters in brain by perfusion with α-(methylamino)-isobutyric acid (MeAIB) or 2-aminobicyclo-(2,2,1)-heptane-2-carboxylic acid (BCH) respectively, was tested. The data showed a significantly greater increase in interstitial fluid Gln upon BCH than MeAIB treatment. Furthermore, brain BCH perfusion also strongly increased the influx of hGln into interstitial fluid following IP injection consistent with transstimulation of LAT1-mediated transendothelial transport. Taken together, the data support the independent homeostatic regulation of amino acids in interstitial fluid vs. cerebrospinal fluid and the role of the blood–brain barrier expressed SLC7A5/LAT1 as a key interstitial fluid gatekeeper.

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Holt, David E., Robert J. Washabau, Sina Djali, Betsy Dayrell-Hart, Kenneth J. Drobatz, Melvyn P. Heyes y Michael B. Robinson. "Cerebrospinal fluid glutamine, tryptophan, and tryptophan metabolite concentrations in dogs with portosystemic shunts". American Journal of Veterinary Research 63, n.º 8 (agosto de 2002): 1167–71. http://dx.doi.org/10.2460/ajvr.2002.63.1167.

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Alfredsson, G., F. A. Wiesel y M. Lindberg. "Glutamate and glutamine in cerebrospinal fluid and serum from healthy volunteers—analytical aspects". Journal of Chromatography B: Biomedical Sciences and Applications 424 (enero de 1988): 378–84. http://dx.doi.org/10.1016/s0378-4347(00)81116-0.

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Ohtake, T., H. Yasuda, H. Takahashi, T. Goto, K. Suzuki, K. Yonemura y A. Hishida. "Decreased plasma and cerebrospinal fluid glutamine concentrations in a patient with bialaphos poisoning". Human & Experimental Toxicology 20, n.º 8 (agosto de 2001): 429–34. http://dx.doi.org/10.1191/096032701682692973.

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A 47-year-old Japanese woman undergoing maintenance hemodialysis (HD) was admitted to our hospital because of poisoning with the herbicide bialaphos. Respiratory arrest and loss of consciousness ensued rapidly, accompanied by convulsions and nystagmus. Treatment with HD and direct hemoperfusion, followed by HD alone, effectively removed bialaphos and its chief toxic metabolite (L-AMPB) from the circulation (bialaphos decreased from 0.33 to <0.05 g/ml andL-AMPBfrom14to0.86 g/ml). The glutamate concentration improved gradually after the removal of bialaphos and L-AMPB from plasma (plasma glutamate concentration: 250.4 nmol/l on day 5 to 120.6 nmol/l on day 26). Decreased glutamine concentration in cerebrospinal fluidwasdemonstratedforthefirsttimeaswellasinplasma, indicating glutaminesynthetase inhibition notonlyinplants but also in humans by bialaphos poisoning.

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Ang, R. C., B. Hoop y H. Kazemi. "Brain glutamate metabolism during metabolic alkalosis and acidosis". Journal of Applied Physiology 73, n.º 6 (1 de diciembre de 1992): 2552–58. http://dx.doi.org/10.1152/jappl.1992.73.6.2552.

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Glutamate modifies ventilation by altering neural excitability centrally. Metabolic acid-base perturbations may also alter cerebral glutamate metabolism locally and thus affect ventilation. Therefore, the effect of metabolic acid-base perturbations on central nervous system glutamate metabolism was studied in pentobarbital-anesthetized dogs under normal acid-base conditions and during isocapnic metabolic alkalosis and acidosis. Cerebrospinal fluid transfer rates of radiotracer [13N]ammonia and of [13N]glutamine synthesized de novo via the reaction glutamate+NH3-->glutamine in brain glia were measured during normal acid-base conditions and after 90 min of acute isocapnic metabolic alkalosis and acidosis. Cerebrospinal fluid [13N]ammonia and [13N]glutamine transfer rates decreased in metabolic acidosis. Maximal glial glutamine efflux rate jm equals 85.6 +/- 9.5 (SE) mumol.l-1 x min-1 in all animals. No difference in jm was observed in metabolic alkalosis or acidosis. Mean cerebral cortical glutamate concentration was significantly lower in acidosis [7.01 +/- 0.45 (SE) mumol/g brain tissue] and tended to be larger in alkalosis, compared with 7.97 +/- 0.89 mumol/g in normal acid-base conditions. There was a similar change in cerebral cortical gamma-aminobutyric acid concentration. Within the limits of the present method and measurements, the results suggest that acute metabolic acidosis but not alkalosis reduces glial glutamine efflux, corresponding to changes in cerebral cortical glutamate metabolism. These results suggest that glutamatergic mechanisms may contribute to central respiratory control in metabolic acidosis.

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Gruenbaum, Shaun E., Roni Dhaher, Kevin Behar, Hitten Zaveri, Mark Erfe y Tore Eid. "2235 15N-Leucine transport across the blood brain barrier is significantly impaired in the glutamine synthetase-inhibited brain". Journal of Clinical and Translational Science 2, S1 (junio de 2018): 1. http://dx.doi.org/10.1017/cts.2018.37.

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OBJECTIVES/SPECIFIC AIMS: Astroglial glutamine synthetase (GS), which metabolizes glutamate and ammonia to glutamine, is critical for the detoxification of brain ammonia, clearance of synaptic glutamate, and production of brain glutamine. Perturbations in the expression and activity of GS are thought to play a causative role in the pathogenesis of several conditions of abnormal neurotransmission. Although the long-term consequences of GS inhibition on amino acid homeostasis in the brain are unknown, it is thought that amino acid influx in the brain is tightly coupled with glutamine efflux via the L-type amino acid transporter. Both glutamine and leucine serve many critical functions in the brain including protein synthesis, gene expression, insulin regulation, and immune signaling. The objective of this study was to determine the effects of chronic GS inhibition with methionine sulfoximine (MSO) on glutamine and leucine homeostasis in the brain. METHODS/STUDY POPULATION: In total, 12 rats were surgically implanted with microdialysis guide cannulas in the bilateral dentate gyrus. Rats were randomly divided for surgical implantation of either a MSO (n=6) or phosphate buffer saline (PBS; n=6) pump in the right dentate gyrus. After 7 days, bilateral microdialysis probes were placed under brief isoflurane anesthesia, and microdialysis flow was established by infusing 0.5 µL/min of artificial extracellular fluid. Dialysate samples were collected every 30 minutes for the duration of the experiment. A 113 mM 15N-Leucine (3.6 mL/h) and 2 M 2–13C-sodium acetate (0.0633 μL/g/min for t=0–5 min, 0.0316 μL/g/min for t=5–10 min, and 0.0253 μL/g/min for t>10 min) solution was infused intravenously for 300 minutes. The EZ:Faast Free Amino Acid analysis kit and ultra-performance liquid chromatography/tandem mass spectrometry was used for quantification of amino acids in the dialysate fluid. RESULTS/ANTICIPATED RESULTS: At baseline (t=0 h), the concentrations of glutamine were significantly lower in MSO-treated rats (p<0.001) in the ipsilateral (GS-inhibited) hippocampus. There were no differences in glutamine concentrations between MSO and PBS-treated rats in the contralateral hippocampus. In PBS-treated rats, there was a significant increase in 15N-leucine between t=0 hour and t=5 hour in the contralateral (p<0.05) and ipsilateral (p<0.05) hippocampus. In MSO-treated rats, there was a significant increase in 15N-leucine between t=0 and t=5 hours in the contralateral (p<0.05) hippocampus, but not in the ipsilateral hippocampus (p=ns.). DISCUSSION/SIGNIFICANCE OF IMPACT: This study demonstrated for the first time that basal glutamine concentrations are low in areas of the brain where GS is acutely inhibited, and that leucine uptake in these brain areas are markedly decreased. Perturbations in glutamine and leucine homeostasis have been implicated in several disease processes including diabetes, obesity, liver disease, immune system dysfunction, epilepsy, and cancer, and the glutamine-dependent leucine influx in the brain may be a novel and important therapeutic target to treat these conditions.

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Saso, Luciano, Maria Grazia Leone, Claudio Sorrentino, Sabrina Giacomelli, Bruno Silvestrini, Josephine Grima, Jonathan Li, Eileen Samy, Dolores Mruk y C. Yan Cheng. "Quantification of prostaglandin D synthetase in cerebrospinal fluid: A potential marker for brain tumor". IUBMB Life 46, n.º 4 (noviembre de 1998): 643–56. http://dx.doi.org/10.1080/15216549800204172.

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Yurdakök, Murat, Safak Göktogan, Gülsen Erdem, Imran Özalp, Gülsevin Tekinalp, Turgay Coskun y Melda Çaglar. "Cerebrospinal fluid glutamine level in the differential diagnosis of a “bloody Tap” in newborn infants". Brain and Development 14, n.º 6 (noviembre de 1992): 428–29. http://dx.doi.org/10.1016/s0387-7604(12)80357-3.

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An, Je Hi, Yuzhuo Su, Thomas Radman y Marom Bikson. "Effects of glucose and glutamine concentration in the formulation of the artificial cerebrospinal fluid (ACSF)". Brain Research 1218 (julio de 2008): 77–86. http://dx.doi.org/10.1016/j.brainres.2008.04.007.

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Camargo, José Augusto y Paulo Henrique Ferreira Bertolucci. "Quantification of Amino Acid Neurotransmitters in Cerebrospinal Fluid of Patients with Neurocysticercosis". Open Neurology Journal 9, n.º 1 (23 de junio de 2015): 15–20. http://dx.doi.org/10.2174/1874205x01509010015.

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Background : Neurocysticercosis is a parasitic disease that affects the central nervous system. Its main clinical manifestations are epileptic seizures. The objective of this study was to investigate the correlation between neurotransmitter concentrations in cerebrospinal fluid (CSF) and the different evolutive forms of neurocysticercosis with or without seizures. Methods : Neurotransmitter concentrations (Aspartate, Glutamate, GABA, Glutamine, Glycine, Taurine) were determined in CSF samples from 42 patients with neurocysticercosis divided into patients with the active cystic form (n = 24, 12 with and 12 without seizures) and patients with calcified form (n = 18, 12 with and 6 without seizures), and a control group consisting of 59 healthy subjects. Results : Alterations in amino acid concentration were observed in all patients with neurocysticercosis. Conclusion : We conclude that disturbances in amino acid metabolism accompany the presentation of neurocysticercosis. Replacement of the terms inactive cyst by reactive inactive cyst and calcification by reactive calcification is suggested.

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Jonung, Torbjörn, Adel Ramzy, Per Herlin, William T. Chance, J. Howard James y Josef E. Fischer. "Factors Influencing the Concentrations of the Large Neutral Amino Acids in the Brain and in the CSF of Dogs After Portacaval Anastomosis". HPB Surgery 4, n.º 4 (1 de enero de 1991): 299–312. http://dx.doi.org/10.1155/1991/53689.

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Portal-systemic shunting of blood is associated with hyperammonemia, an increased glutamine concentration in brain, an altered plasma neutral amino acid pattern, and high levels of several of the large neutral amino acids in brain. Since some of these amino acids are precursors for neurotransmitters and for other potentially neuroactive substances, high CNS levels of these amino acids may contribute to the development of encephalopathy. In order to determine the relative importance of changes in brain glutamine levels and changes in competition among the neutral amino acids for blood-brain transport, we measured the concentrations of the large neutral amino acids in plasma, cisternal cerebrospinal fluid and in brain tissue from various regions of dogs after end-to-side portacaval shunt. Although the changes in CSF amino acid levels correlated partially with altered amino acid plasma competitor ratios, better correlations were observed with the elevation of CSF glutamine. These results suggest a model of blood-brain amino acid transport in which a high level of glutamine in brain extracellular fluid competes with other neutral amino acids for efflux from brain, thus raising brain amino acid levels after portalsystemic shunting

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Bell, Jimmy D., Judith C. C. Brown, Peter J. Sadler, Andrew F. MacLeod, Peter H. Sönksen, Robin D. Hughes y Roger Williams. "High resolution proton nuclear magnetic resonance studies of human cerebrospinal fluid". Clinical Science 72, n.º 5 (1 de mayo de 1987): 563–70. http://dx.doi.org/10.1042/cs0720563.

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1. One- and two-dimensional (correlated shift spectroscopy) high resolution proton n.m.r. spectra of human cerebrospinal fluid (CSF) are reported. The merits of water suppression by freeze drying or irradiation, and spectral simplification by spin-echo methods, are discussed. 2. Well-resolved resonances for a range of low molecular weight metabolites such as lactate, 3-d-hydroxybutyrate, alanine, acetate, citrate, glucose, valine and formate were observed. Resonances for glutamine were observed only from freeze dried samples. Concentrations determined by n.m.r. were in reasonable agreement with those from conventional methods. 3. The n.m.r. spectra of CSF were related to the clinical conditions of the subjects. No resonances for citrate were present in spectra of CSF from subjects (three infants) with bacterial meningitis; high lactate and lowered glucose levels were observed. Strong resonances for glucose and glycine were observed for mildly diabetic subjects. Both the aromatic and the aliphatic regions of the CSF spectra from subjects suffering from liver failure contained distinctive features characteristic for hepatic coma: intense resonances for lactate, alanine, valine, methionine, tyrosine, phenylalanine and histidine. In some cases guanine was also present, which does not appear to have been reported previously. The two-dimensional spectrum suggested the presence of abnormally high levels of a number of endogenous metabolites. Such assignments were not possible using one-dimensional spectra alone because of signal overlap.

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Vargas, C., M. Tannhauser y H. M. T. Barros. "Dissimilar Effects of Lithium and Valproic Acid on GABA and Glutamine Concentrations in Rat Cerebrospinal Fluid". General Pharmacology: The Vascular System 30, n.º 4 (abril de 1998): 601–4. http://dx.doi.org/10.1016/s0306-3623(97)00328-5.

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Atkinson, D. E. y E. Bourke. "Metabolic aspects of the regulation of systemic pH". American Journal of Physiology-Renal Physiology 252, n.º 6 (1 de junio de 1987): F947—F956. http://dx.doi.org/10.1152/ajprenal.1987.252.6.f947.

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Catabolism of protein produces CO2, NH4+, and HCO3-. Mammals readily lose CO2 through the lungs, but the bicarbonate produced in metabolism of a typical diet (in humans, approximately 1 mol/day from approximately 100 g of protein) would cause alkalosis if not disposed of. Air-breathing animals solve this problem by incorporating NH4+ into organic compounds in which N is not protonated; thus each NH4+ ion loses a proton in the course of the synthesis. These protons serve to titrate HCO3-. In mammals, ureagenesis is the pathway by which protons are liberated from NH4+. The rate of ureagenesis therefore determines the rate of disposal of bicarbonate, and must be an important factor in the maintenance of pH homeostasis. Ammonium ion that is not needed for urea synthesis is packaged into glutamine by the liver. Hepatic glutamine synthetase is localized in the last rank of cells around the pericentral venule; thus glutamine synthetase cannot compete for NH4+ or interfere with the control of pH by urea synthesis. Ammonium excretion in the urine does not represent excretion of acid, and is not stoichiometrically related to renal generation of bicarbonate. The quantitatively major processes by which the HCO3-/CO2 ratio, and hence the pH, is regulated in blood and interstitial fluid are excretion of CO2 through the lungs and disposal of HCO3- as a consequence of ureagenesis in the liver.

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Okada, Toshiki, Yukinaga Watanabe, Saul W. Brusilow, Richard J. Traystman y Raymond C. Koehler. "Interaction of glutamine and arginine on cerebrovascular reactivity to hypercapnia". American Journal of Physiology-Heart and Circulatory Physiology 278, n.º 5 (1 de mayo de 2000): H1577—H1584. http://dx.doi.org/10.1152/ajpheart.2000.278.5.h1577.

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Glutamine is purported to inhibit recycling of citrulline to arginine and to limit nitric oxide release in vitro. However, vasoactive effects of glutamine have not been clearly demonstrated in vivo. During hyperammonemia, impaired cerebrovascular reactivity to CO2 is related to glutamine accumulation. We tested the hypotheses that 1) glutamine infusion in the absence of hyperammonemia impairs cerebrovascular CO2 reactivity and 2) arginine infusion preserves CO2 reactivity during glutamine infusion and during hyperammonemia. Pentobarbital sodium-anesthetized rats were equipped with a closed cranial window for measuring pial arteriolar diameter. Intravenous infusion of 3 mmol ⋅ kg− 1 ⋅ h− 1of l-glutamine for 6 h produced threefold increases in plasma and cerebrospinal fluid concentrations. Dilation to hypercapnia was reduced by 45% compared with that of a time control group at 6 h but not at 3 h of glutamine infusion. Coinfusion of 2 mmol ⋅ kg− 1 ⋅ h− 1of l-arginine with glutamine maintained the hypercapnic vasodilation at the control value. Infusion of ammonium acetate at a rate known to produce threefold increases in cortical tissue glutamine concentration resulted in no significant hypercapnic vasodilation. Coinfusion of arginine with ammonium acetate maintained hypercapnic vasodilation at 60% of the control value. Arginine infusion did not augment hypercapnic vasodilation in a control group. We conclude that glutamine modulates cerebrovascular CO2 reactivity in vivo. Glutamine probably acts by limiting arginine availability because the vascular inhibitory effect required >3 h to develop and because arginine infusion counteracted the vascular effect of both endogenously and exogenously produced increases in glutamine.

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Kleerekooper, Iris, Megan K. Herbert, H. Bea Kuiperij, Douglas Kazutoshi Sato, Kazuo Fujihara, Dagoberto Callegaro, Romain Marignier et al. "CSF levels of glutamine synthetase and GFAP to explore astrocytic damage in seronegative NMOSD". Journal of Neurology, Neurosurgery & Psychiatry 91, n.º 6 (26 de marzo de 2020): 605–11. http://dx.doi.org/10.1136/jnnp-2019-322286.

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ObjectiveTo explore levels of astrocytopathy in neuromyelitis optica spectrum disorder (NMOSD) by measuring levels of the astrocytic enzyme glutamine synthetase (GS) and glial fibrillary acidic protein (GFAP), an established astrocytic biomarker known to be associated with disease activity in multiple sclerosis.MethodsCerebrospinal fluid concentrations of GS and GFAP were measured by ELISA in patients with NMOSD (n=39, 28 aquaporin-4 (AQP4)-Ab-seropositive, 3 double-Ab-seronegative, 4 myelin oligodendrocyte glycoprotein (MOG)-Ab-seropositive and 4 AQP4-Ab-seronegative with unknown MOG-Ab-serostatus), multiple sclerosis (MS) (n=69), optic neuritis (n=5) and non-neurological controls (n=37).ResultsGFAP and GS concentrations differed significantly across groups (both p<0.001), showing a similar pattern of elevation in patients with AQP4-Ab-seropositive NMOSD. GS and GFAP were significantly correlated, particularly in patients with AQP4-Ab-seropositive NMOSD (rs=0.70, p<0.001). Interestingly, GFAP levels in some patients with double-Ab-seronegative NMOSD were markedly increased.ConclusionsOur data indicate astrocytic injury occurs in some patients with double-Ab-seronegative NMOSD, which hints at the possible existence of yet undiscovered astrocytic autoimmune targets. We hypothesise that elevated GS and GFAP levels could identify those double-Ab-seronegative patients suitable to undergo in-depth autoimmune screening for astrocytic antibodies.

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Joanna, Lynch, Peeling James, Auty Anthony y R. Sutherland Garnette. "Nuclear Magnetic Resonance Study of Cerebrospinal Fluid From Patients With Multiple Sclerosis". Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 20, n.º 3 (agosto de 1993): 194–98. http://dx.doi.org/10.1017/s0317167100047922.

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ABSTRACT:Proton nuclear magnetic resonance (NMR) spectroscopy was used to examine cerebrospinal fluid (CSF) from patients (n = 30) with actively progressive multiple sclerosis (MS). Metabolite concentrations obtained from the spectra were compared to those determined from the spectra of CSF from control patients (n = 27) with benign spinal disorders. No significant difference was found between the 2 groups for most constituents, including lactate, glutamine, citrate, creatine and creatinine, and glucose. Acetate levels were significantly higher in MS patients, while formate levels were significantly lower, than the controls. There were no significant differences in metabolite concentrations in CSF from early and longstanding MS patients. A peak due to an unidentified compound was found at 2.82 ppm in the spectra of CSF from patients with actively progressive MS, but not in the spectra of CSF from the controls. The peak was not found in spectra of CSF from patients with AIDS dementia complex (n = 9) or Parkinson's disease (n = 5), but it did appear in spectra of CSF from 1 patient with Jakob-Creutzfeldt disease (out of 3 examined) and from 1 patient (out of 7) with Guillan-Barré disease. The unidentified compound is volatile and, from the chemical shift of the observed NMR peak, is probably an N-methyl compound. As such, it may be an intermediate in the cholino-glycine cycle, in which an abnormality has been proposed to exist in MS patients.

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Herman, Stephanie, Torbjörn Åkerfeldt, Ola Spjuth, Joachim Burman y Kim Kultima. "Biochemical Differences in Cerebrospinal Fluid between Secondary Progressive and Relapsing–Remitting Multiple Sclerosis". Cells 8, n.º 2 (24 de enero de 2019): 84. http://dx.doi.org/10.3390/cells8020084.

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To better understand the pathophysiological differences between secondary progressive multiple sclerosis (SPMS) and relapsing-remitting multiple sclerosis (RRMS), and to identify potential biomarkers of disease progression, we applied high-resolution mass spectrometry (HRMS) to investigate the metabolome of cerebrospinal fluid (CSF). The biochemical differences were determined using partial least squares discriminant analysis (PLS-DA) and connected to biochemical pathways as well as associated to clinical and radiological measures. Tryptophan metabolism was significantly altered, with perturbed levels of kynurenate, 5-hydroxytryptophan, 5-hydroxyindoleacetate, and N-acetylserotonin in SPMS patients compared with RRMS and controls. SPMS patients had altered kynurenine compared with RRMS patients, and altered indole-3-acetate compared with controls. Regarding the pyrimidine metabolism, SPMS patients had altered levels of uridine and deoxyuridine compared with RRMS and controls, and altered thymine and glutamine compared with RRMS patients. Metabolites from the pyrimidine metabolism were significantly associated with disability, disease activity and brain atrophy, making them of particular interest for understanding the disease mechanisms and as markers of disease progression. Overall, these findings are of importance for the characterization of the molecular pathogenesis of SPMS and support the hypothesis that the CSF metabolome may be used to explore changes that occur in the transition between the RRMS and SPMS pathologies.

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La Heij, Ellen C., Marjo P. H. Van De Waarenburg, Harriet G. T. Blaauwgeers, Alfons G. H. Kessels, Jan De Vente, Albert T. A. Liem, Harry Steinbusch y Fred Hendrikse. "Levels of basic fibroblast growth factor, glutamine synthetase, and interleukin-6 in subretinal fluid from patients with retinal detachment". American Journal of Ophthalmology 132, n.º 4 (octubre de 2001): 544–50. http://dx.doi.org/10.1016/s0002-9394(01)01125-4.

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Hoop, B., D. M. Systrom, V. E. Shih y H. Kazemi. "Central respiratory effects of glutamine synthesis inhibition in dogs". Journal of Applied Physiology 65, n.º 3 (1 de septiembre de 1988): 1099–109. http://dx.doi.org/10.1152/jappl.1988.65.3.1099.

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Glutamic acid is an excitatory neurotransmitter that may have a significant role in the central chemical drive of ventilation. Therefore cardiorespiratory function was measured in pentobarbital sodium-anesthetized dogs before and after central inhibition of glutamate metabolism by means of methionine sulfoximine (MSO), a specific inhibitor of glutamine synthase (GS) catalyzing amidation of glutamate to glutamine. GS was inhibited centrally by perfusing the ventriculocisternal space with artificial cerebrospinal fluid (CSF) containing 92.5 mmol MSO per liter at a fixed pH, perfusion rate, and pressure. After GS inhibition, CSF transfer rate of [13N]glutamine synthesized from 13NH4+ amidation of glutamate was reduced five-fold, and minute ventilation increased from 2.90 +/- 0.41 (SE) l/min (0.164 +/- 0.020 l.min-1.kg body wt-1) to 4.46 +/- 0.52 l/min (0.254 +/- 0.029 l.min-1.kg body wt-1). This increase in ventilation with endogenous glutamate and the increase in ventilation previously observed during ventriculocisternal perfusion of exogenous glutamate are compared quantitatively via a model of central neurotransmitter glutamate chemoreception. The results support the hypothesis that the endogenous brain glutamate is important in the central chemical drive of ventilation.

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Yarema, C., H. McLean y S. Caveney. "l-Glutamate retrieved with the moulting fluid is processed by a glutamine synthetase in the pupal midgut of Calpodes ethlius". Journal of Insect Physiology 46, n.º 11 (noviembre de 2000): 1497–507. http://dx.doi.org/10.1016/s0022-1910(00)00075-5.

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Hoop, B., M. R. Masjedi, V. E. Shih y H. Kazemi. "Brain glutamate metabolism during hypoxia and peripheral chemodenervation". Journal of Applied Physiology 69, n.º 1 (1 de julio de 1990): 147–54. http://dx.doi.org/10.1152/jappl.1990.69.1.147.

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Glutamate stimulates resting ventilation by altering neural excitability centrally. Hypoxia increases central ventilatory drive through peripheral chemoreceptor stimulation and may also alter cerebral perfusion and glutamate metabolism locally. Therefore the effect of hypoxia and peripheral chemodenervation on cerebrospinal fluid (CSF) transfer rate of in vivo tracer amidated central nervous system glutamate was studied in intact and chemodenervated pentobarbital-anesthetized dogs during normoxia and after 1 h of hypoxia induced with 10 or 12% O2 in N2 breathing at constant expired ventilation and arterial CO2 tension. Chemodenervation was performed by bilateral sectioning of the carotid body nerves and cervical vagi. CSF transfer rates of radiotracer 13NH4+ and [13N]glutamine synthesized via the reaction, glutamate + NH4(+)----glutamine, in brain glia were measured during normoxia and after 1 h of hypoxia. At normoxia, maximal glial glutamine efflux rate jm = 103.3 +/- 11.2 (SE) mumol.l-1.min-1 in all animals. After 1 h of hypoxia in intact animals, jm = 78.4 +/- 10.0 mumol.l-1.min-1. In denervated animals, jm was decreased to 46.3 +/- 4.3 mumol.l-1.min-1. During hypoxia, mean cerebral cortical glutamate concentration was higher in denervated animals (9.98 +/- 1.43 mumol/g brain tissue) than in intact animals (7.63 +/- 1.82 mumol/g brain tissue) and corresponding medullary glutamate concentration tended to be higher in denervated animals. There were no differences between mean glutamine and gamma-aminobutyric acid concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

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SAKATOKU, HIROYUKI, MASAKAZU INOUE, MASAMITSU KOJIMA, EIICHI AZUMA, YOSHIHIRO KOMADA, YAN-WEN ZHOU, SHAO-LI ZHANG y MINORU SAKURAI. "2‘,5’-oligoadenylate synthetase activity and T cell subset in the cerebrospinal fluid and peripheral blood of aseptic meningitis". Pediatrics International 39, n.º 1 (febrero de 1997): 48–53. http://dx.doi.org/10.1111/j.1442-200x.1997.tb03555.x.

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Zhou, Yun, Leonie F. Waanders, Silvia Holmseth, Caiying Guo, Urs V. Berger, Yuchuan Li, Anne-Catherine Lehre, Knut P. Lehre y Niels C. Danbolt. "Proteome Analysis and Conditional Deletion of the EAAT2 Glutamate Transporter Provide Evidence against a Role of EAAT2 in Pancreatic Insulin Secretion in Mice". Journal of Biological Chemistry 289, n.º 3 (26 de noviembre de 2013): 1329–44. http://dx.doi.org/10.1074/jbc.m113.529065.

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Islet function is incompletely understood in part because key steps in glutamate handling remain undetermined. The glutamate (excitatory amino acid) transporter 2 (EAAT2; Slc1a2) has been hypothesized to (a) provide islet cells with glutamate, (b) protect islet cells against high extracellular glutamate concentrations, (c) mediate glutamate release, or (d) control the pH inside insulin secretory granules. Here we floxed the EAAT2 gene to produce the first conditional EAAT2 knock-out mice. Crossing with Nestin-cyclization recombinase (Cre) eliminated EAAT2 from the brain, resulting in epilepsy and premature death, confirming the importance of EAAT2 for brain function and validating the genetic construction. Crossing with insulin-Cre lines (RIP-Cre and IPF1-Cre) to obtain pancreas-selective deletion did not appear to affect survival, growth, glucose tolerance, or β-cell number. We found (using TaqMan RT-PCR, immunoblotting, immunocytochemistry, and proteome analysis) that the EAAT2 levels were too low to support any of the four hypothesized functions. The proteome analysis detected more than 7,000 islet proteins of which more than 100 were transporters. Although mitochondrial glutamate transporters and transporters for neutral amino acids were present at high levels, all other transporters with known ability to transport glutamate were strikingly absent. Glutamate-metabolizing enzymes were abundant. The level of glutamine synthetase was 2 orders of magnitude higher than that of glutaminase. Taken together this suggests that the uptake of glutamate by islets from the extracellular fluid is insignificant and that glutamate is intracellularly produced. Glutamine synthetase may be more important for islets than assumed previously.

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Eckstein, James A., Gina M. Ammerman, Jessica M. Reveles y Bradley L. Ackermann. "Analysis of glutamine, glutamate, pyroglutamate, and GABA in cerebrospinal fluid using ion pairing HPLC with positive electrospray LC/MS/MS". Journal of Neuroscience Methods 171, n.º 2 (junio de 2008): 190–96. http://dx.doi.org/10.1016/j.jneumeth.2008.02.019.

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Tucci, Sonia, Claudio Pinto, Jose Goyo, Pedro Rada y Luis Hernández. "Measurement of Glutamine and Glutamate by Capillary Electrophoresis and Laser Induced Fluorescence Detection in Cerebrospinal Fluid of Meningitis Sick Children". Clinical Biochemistry 31, n.º 3 (abril de 1998): 143–50. http://dx.doi.org/10.1016/s0009-9120(98)00003-4.

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Kato, Masaru, HongMei Jin, Kumiko Sakai-Kato, Toshimasa Toyo’oka, Maria T. Dulay y Richard N. Zare. "Determination of glutamine and serine in rat cerebrospinal fluid using capillary electrochromatography with a modified photopolymerized sol–gel monolithic column". Journal of Chromatography A 1004, n.º 1-2 (julio de 2003): 209–15. http://dx.doi.org/10.1016/s0021-9673(03)00451-5.

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Dahlberg, Daniel, Eduard A. Struys, Erwin E. Jansen, Lars Mørkrid, Øivind Midttun y Bjørnar Hassel. "Cyst Fluid From Cystic, Malignant Brain Tumors: A Reservoir of Nutrients, Including Growth Factor-Like Nutrients, for Tumor Cells". Neurosurgery 80, n.º 6 (25 de enero de 2017): 917–24. http://dx.doi.org/10.1093/neuros/nyw101.

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Abstract BACKGROUND: Brain tumors may have cysts, whose content of nutrients could influence tumor cell microenvironment and growth. OBJECTIVE: To measure nutrients in cyst fluid from glioblastoma multiforme (GBM) and metastatic brain tumors. METHODS: Quantification of nutrients in cyst fluid from 12 to 18 GBMs and 4 to 10 metastatic brain tumors. RESULTS: GBM cysts contained glucose at 2.2 mmol/L (median value; range <0.8-3.5) and glutamine at 1.04 mmol/L (0.17-4.2). Lactate was 7.1 mmol/L (2.4-12.5) and correlated inversely with glucose level (r = –0.77; P < .001). Amino acids, including glutamate, varied greatly, but median values were similar to previously published serum values. Ammonia was 75 μmol/L (11-241). B vitamins were present at previously published serum values, and riboflavin, nicotinamide, pyridoxal 5΄-phosphate, and cobalamin were higher in cyst fluid than in cerebrospinal fluid. Inorganic phosphate was 1.25 mmol/L (0.34-3.44), which was >3 times higher than in ventricular cerebrospinal fluid: 0.35 mmol/L (0.22-0.66; P < .001). Tricarboxylic acid cycle intermediates were in the low micromolar range, except for citrate, which was 240 μmol/L (140-590). In cystic metastatic malignant melanomas and lung tumors values were similar to those in GBMs. CONCLUSION: Tumor cysts may be a nutrient reservoir for brain tumors, securing tumor energy metabolism and synthesis of cell constituents. Serum is one likely source of cyst fluid nutrients. Nutrient levels in tumor cyst fluid are highly variable, which could differentially stimulate tumor growth. Cyst fluid glutamate, lactate, and phosphate may act as tumor growth factors; these compounds have previously been shown to stimulate tumor growth at concentrations found in tumor cyst fluid.

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Härtel, Tobias, Matthias Klein, Uwe Koedel, Manfred Rohde, Lothar Petruschka y Sven Hammerschmidt. "Impact of Glutamine Transporters on Pneumococcal Fitness under Infection-Related Conditions". Infection and Immunity 79, n.º 1 (15 de noviembre de 2010): 44–58. http://dx.doi.org/10.1128/iai.00855-10.

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ABSTRACTThe genomic analysis ofStreptococcuspneumoniaepredicted six putative glutamine uptake systems, which are expressed underinvitroconditions, as shown here by reverse transcription-PCR. Four of these operons consist ofglnHPQ, while two lackglnH, which encodes a soluble glutamine-binding protein. Here, we studied the impact of two of these glutamine ATP-binding cassette transporters onS.pneumoniaeD39 virulence and phagocytosis, which consist of GlnQ and a translationally fused protein of GlnH and GlnP. Mice infected intranasally with D39Δgln0411/0412showed significantly increased survival times and a significant delay in the development of pneumococcal pneumonia compared to those infected with D39, as observed in real time using bioluminescent pneumococci. In a mouse sepsis model, the mutant D39Δgln0411/0412showed only moderate but significant attenuation. In contrast, the D39Δgln1098/1099knockout strain was massively attenuated in the pneumonia and septicemia mouse infection model. To cause pneumonia or sepsis with D39Δgln1098/1099, infection doses 100- to 10,000-fold higher than those used for wild-type strain D39 were required. In an experimental mouse meningitis model, D39Δgln1098/1099produced decreased levels of white blood cells in cerebrospinal fluid and showed decreased numbers of bacteria in the bloodstream compared to D39 and D39Δgln0411/0412. Phagocytosis experiments revealed significantly decreased intracellular survival rates of mutants D39Δgln1098/1099and D39Δgln0411/0412compared to wild-type D39, suggesting that the deficiency of Gln uptake systems impairs resistance to oxidative stress. Taken together, our results demonstrate that both glutamine uptake systems are required for full virulence of pneumococci but exhibit different impacts on the pathogenesis of pneumococci underinvivoconditions.

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La Heij, Ellen C., Marjo P. H. van de Waarenburg, Harriet G. T. Blaauwgeers, Alfons G. H. Kessels, Albert T. A. Liem, Charlotte Theunissen, Harry Steinbusch y Fred Hendrikse. "Basic fibroblast growth factor, glutamine synthetase, and interleukin-6 in vitreous fluid from eyes with retinal detachment complicated by proliferative vitreoretinopathy". American Journal of Ophthalmology 134, n.º 3 (septiembre de 2002): 367–75. http://dx.doi.org/10.1016/s0002-9394(02)01536-2.

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Aasly, Jan O., Oddbjørn Sæther, Krisztina K. Johansen, Tone F. Bathen, Guro F. Giskeødegård y Linda R. White. "Changes to Intermediary Metabolites in Sporadic andLRRK2Parkinson’s Disease Demonstrated by Proton Magnetic Resonance Spectroscopy". Parkinson's Disease 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/264896.

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Background. Parkinson’s disease (PD) remains a clinical diagnosis and biomarkers are needed to detect the disease as early as possible. Genetically determined PD provides an opportunity for studying metabolic differences in connection with disease development.Objectives. To study the levels of intermediary metabolites in cerebrospinal fluid (CSF) from patients with PD, either of sporadic type or in carriers of theLRRK2p.G2019S mutation.Methods. Results from patients with sporadic PD orLRRK2-PD were compared with asymptomaticLRRK2mutation carriers and healthy control individuals. CSF was analysed by proton MR spectroscopy (1H-MRS) giving reliable results for 16 intermediary metabolites. Partial least squares discriminant analysis (PLS-DA) was applied to study group differences.Results. PLS-DA distinguished PD patients from healthy individuals based on the metabolites identified in CSF, with 2-hydroxybutyrate, glutamine, and dimethyl sulphone largely contributing to the separations.Conclusion. Speculatively, all three metabolites could alter concentration in response to metabolic changes connected with neurodegeneration; glutamine as a means of removing excess nitrogen from brain, dimethyl sulphone as an anti-inflammatory agent, and 2-hydroxybutyrate in connection with altered glutathione metabolism. Potentially,1H-MRS is a promising tool for identifying novel biomarkers for PD.

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Jung, Carla S., Bettina Lange, Michael Zimmermann y Volker Seifert. "CSF and Serum Biomarkers Focusing on Cerebral Vasospasm and Ischemia after Subarachnoid Hemorrhage". Stroke Research and Treatment 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/560305.

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Delayed cerebral vasospasm (CVS) and delayed cerebral ischemia (DCI) remain severe complications after subarachnoid hemorrhage (SAH). Although focal changes in cerebral metabolism indicating ischemia are detectable by microdialysis, routinely used biomarkers are missing. We therefore sought to evaluate a panel of possible global markers in serum and cerebrospinal fluid (CSF) of patients after SAH. CSF and serum of SAH patients were analyzed retrospectively. In CSF, levels of inhibitory, excitatory, and structural amino acids were detected by high-performance liquid chromatography (HPLC). In serum, neuron-specific enolase (NSE) and S100B level were measured and examined in conjunction with CVS and DCI. CVS was detected by arteriography, and ischemic lesions were assessed by computed tomography (CT) scans. All CSF amino acids were altered after SAH. CSF glutamate, glutamine, glycine, and histidine were significantly correlated with arteriographic CVS. CSF glutamate and serum S100B were significantly correlated with ischemic events after SAH; however, NSE did not correlate neither with ischemia nor with vasospasm. Glutamate, glutamine, glycine, and histidine might be used in CSF as markers for CVS. Glutamate also indicates ischemia. Serum S100B, but not NSE, is a suitable marker for ischemia. These results need to be validated in larger prospective cohorts.

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Goldsmith, R. F., J. W. Earl y A. M. Cunningham. "Determination of delta-aminobutyric acid and other amino acids in cerebrospinal fluid of pediatric patients by reversed-phase liquid chromatography." Clinical Chemistry 33, n.º 10 (1 de octubre de 1987): 1736–40. http://dx.doi.org/10.1093/clinchem/33.10.1736.

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Abstract The reversed-phase liquid-chromatographic system described here is capable of resolving the neurotransmitter amino acids aspartic acid, glutamic acid, and gamma-aminobutyric acid (GABA) plus 21 other amino acids in cerebrospinal fluid (CSF) in a single analysis. The amino acids, derivatized with o-phthalaldehyde, are separated in 65 min. Concentrations of glutamine less than or equal to 600 mumol/L can be measured at the same time as GABA greater than or equal to 10 nmol/L. Using this method, we have determined reference intervals for amino acids, including GABA, in CSF in a group of pediatric patients who underwent lumbar puncture before myelography, and who were subsequently shown to have normal myelograms. These intervals are generally lower than those previously reported for childhood, but we believe this results from a more rigid selection of the control group. In addition, artifactual increases in concentrations of free neurotransmitters, caused by breakdown of amino acid conjugates, are minimized by (a) immediate freezing of the CSF samples to prevent enzyme-mediated changes, (b) omission of a deproteinization step, and (c) precolumn derivatization to reduce on-column breakdown of amide and peptide forms.

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Murgia, Federica, Lorena Lorefice, Simone Poddighe, Giuseppe Fenu, Maria Antonietta Secci, Maria Giovanna Marrosu, Eleonora Cocco y Luigi Atzori. "Multi-Platform Characterization of Cerebrospinal Fluid and Serum Metabolome of Patients Affected by Relapsing–Remitting and Primary Progressive Multiple Sclerosis". Journal of Clinical Medicine 9, n.º 3 (21 de marzo de 2020): 863. http://dx.doi.org/10.3390/jcm9030863.

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Background: Multiple sclerosis (MS) is a chronic immunemediated disease of the central nervous system with a highly variable clinical presentation and disease progression. In this study, we investigate the metabolomics profile of patients affected by relapsing–remitting MS (RRMS)and primary progressive MS (PPMS), in order to find potential biomarkers to distinguish between the two forms. Methods: Cerebrospinal Fluid CSF and blood samples of 34 patients (RRMS n = 22, PPMS n = 12) were collected. Nuclear magnetic resonance (1H-NMR) and mass spectrometry (coupled with a gas chromatography and liquid chromatography) were used as analytical techniques. Subsequently, a multivariate statistical analysis was performed; the resulting significant variables underwent U-Mann–Whitney test and correction for multiple comparisons. Receiver Operating Characteristic ROC curves were built and the pathways analysis was conducted. Results: The analysis of the serum and the CSF of the two classes, allowed the identification of several altered metabolites (lipids, biogenic amines, and amino acids). The pathways analysis indicated the following pathways were affected: Glutathione metabolism, nitrogen metabolism, glutamine–glutamate metabolism, arginine–ornithine metabolism, phenylalanine, tyrosine and tryptophan biosynthesis etc. Conclusion: The analysis allowed the identification of a set of metabolites able to classify RRMS and PPMS patients, each of whom express different patterns of metabolites in the two biofluids.

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Aas, Jan-Erik, Jon Berg-Johnsen, Elisabeth Hegstad, Jon H. Laake, Iver A. Langmoen y Ole P. Ottersen. "Redistribution of Glutamate and Glutamine in Slices of Human Neocortex Exposed to Combined Hypoxia and Glucose Deprivation in vitro". Journal of Cerebral Blood Flow & Metabolism 13, n.º 3 (mayo de 1993): 503–15. http://dx.doi.org/10.1038/jcbfm.1993.65.

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This study was undertaken to elucidate the roles of neurons and glial cells in the handling of glutamate and glutamine, a glutamate precursor, during cerebral ischemia. Slices (400–600 μm) from human neocortex obtained during surgery for epilepsy or brain tumors were incubated in artificial cerebrospinal fluid and subjected to 30 min of combined hypoxia and glucose deprivation (an in vitro model of brain ischemia). These slices, and control slices that had not been subjected to “ischemic” conditions, were then fixed and embedded. Ultrathin sections were processed according to a postembedding immunocytochemical method with polyclonal antibodies raised against glutamate or glutamine, followed by colloidal gold-labeled secondary antibodies. The gold particle densities over various tissue profiles were calculated from electron micrographs using a specially designed computer program. Combined hypoxia and glucose deprivation caused a reduced glutamate immunolabeling in neuronal somata, while that of glial processes increased. Following 1 h of recovery, the glutamate labeling of neuronal somata declined further to very low values, compared to control slices. The glutamate labeling of glial cells returned to normal levels following recovery. In axon terminals, no consistent change in the level of glutamate immunolabeling was observed. Immunolabeling of glutamine was low in both nerve terminals and neuronal somata in normal slices and was reduced to nondetectable levels in nerve terminals upon hypoxia and glucose deprivation. This treatment was also associated with a reduced glutamine immunolabeling in glial cells. Reversed glutamate uptake due to perturbations of the transmembrane ion concentrations and membrane potential probably contributes to the loss of neuronal glutamate under “ischemic” conditions. The increased glutamate labeling of glial cells under the same conditions can best be explained by assuming that glial cells resist a reversal of glutamate uptake, and that their ability to convert glutamate into glutamine is compromised due to the energy failure. The persistence of a nerve terminal pool of glutamate is compatible with recent biochemical data indicating that the exocytotic glutamate release is contingent on an adequate energy supply and therefore impeded during ischemia.

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