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Jean-claude Rostain - One of the best experts on this subject based on the ideXlab platform.
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neurochemistry of pressure induced nitrogen and metabolically inert gas Narcosis in the central nervous system
Comprehensive Physiology, 2016Co-Authors: Jean-claude Rostain, Cécile LavouteAbstract:Gases that are not metabolized by the organism are thus chemically inactive under normal conditions. Such gases include the "noble gases" of the Periodic Table as well as hydrogen and nitrogen. At increasing pressure, nitrogen induces Narcosis at 4 absolute atmospheres (ATAs) and more in humans and at 11 ATA and more in rats. Electrophysiological and neuropharmacological studies suggest that the striatum is a target of nitrogen Narcosis. Glutamate and dopamine release from the striatum in rats are decreased by exposure to nitrogen at a pressure of 31 ATA (75% of the anesthetic threshold). Striatal dopamine levels decrease during exposure to compressed argon, an inert gas more narcotic than nitrogen, or to nitrous oxide, an anesthetic gas. Inversely, striatal dopamine levels increase during exposure to compressed helium, an inert gas with a very low narcotic potency. Exposure to nitrogen at high pressure does not change N-methyl-d-aspartate (NMDA) glutamate receptor activities in Substantia Nigra compacta and striatum but enhances gama amino butyric acidA (GABAA) receptor activities in Substantia Nigra compacta. The decrease in striatal dopamine levels in response to hyperbaric nitrogen exposure is suppressed by recurrent exposure to nitrogen Narcosis, and dopamine levels increase after four or five exposures. This change, the lack of improvement of motor disturbances, the desensitization of GABAA receptors on dopamine cells during recurrent exposures and the long-lasting decrease of glutamate coupled with the higher sensitivity of NMDA receptors, suggest a nitrogen toxicity induced by repetitive exposures to Narcosis. These differential changes in different neurotransmitter receptors would support the binding protein theory. © 2016 American Physiological Society. Compr Physiol 6:1579-1590, 2016.
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A review of recent neurochemical data on inert gas Narcosis.
Undersea & hyperbaric medicine : journal of the Undersea and Hyperbaric Medical Society Inc, 2011Co-Authors: Jean-claude Rostain, J.j. Risso, Cécile Lavoute, N Vallee, M WeissAbstract:Nitrogen Narcosis occurs in humans at around 0.4 MPa (4 ATA). Hydrogen Narcosis occurs between 2.6 and 3.0 MPa. In rats, nitrogen disturbances occur from 1 MPa and a loss of righting reflex around 4 MPa. Neurochemical studies in striatum of rats with nitrogen at 3 MPa (75% of anesthesia threshold) with differential pulse voltammetry have demonstrated a decrease in dopamine (DA) release by neurons originated from the substantia nigra pars compacta (SNc). Such a decrease is found also with compressed argon, which is more narcotic than nitrogen and with the anesthetic gas nitrous oxide. Inversely, compressed helium with its very low narcotic potency induces DA increase. Microdialysis studies in the striatum have indicated that nitrogen also induces a decrease of glutamate concentration. Nitrogen pressure did not modify NMDA glutamate receptor activities in SNc or striatum but enhanced GABAA receptors activities in SNc. Repetitive exposures to nitrogen Narcosis suppressed the DA decrease and induced an increase. This fact and the lack of improvement of motor disturbances did not support the hypothesis of a physiological adaptation. The desensitization of the GABAA receptors on DA cells during recurrent exposures and the parallel long-lasting decrease of glutamate coupled to the increase in NMDA receptor sensitivity suggest a nitrogen neurotoxicity or addiction induced by recurrent exposures. The differential changes produced by inert gases in different neurotransmitter receptors would support the binding protein theory. n
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Comparison of Nitrogen Narcosis and Helium Pressure Effects on Striatal Amino Acids: A Microdialysis Study in Rats
Neurochemical Research, 2009Co-Authors: Nicolas Vallee, Jean-claude Rostain, Alain Boussuges, Jean-jacques RissoAbstract:Exposure to nitrogen–oxygen mixture at high pressure induces Narcosis, which can be considered as a first step toward general anaesthesia. Narcotic potencies of inert gases are attributed to their lipid solubility. Nitrogen Narcosis induces cognitive and motor disturbances that occur from 0.3 MPa in man and from 1 MPa in rats. Neurochemical studies performed in rats up to 3 MPa have shown that nitrogen pressure decreases striatal dopamine release like argon, another inert gas, or nitrous oxide, an anaesthetic gas. Striatal dopamine release is under glutamatergic and other amino acid neurotransmission regulations. The aim of this work was to study the effects of nitrogen at 3 MPa on striatal amino acid levels and to compare to those of 3 MPa of helium which is not narcotic at this pressure, by using a new technique of microdialysis samples extraction under hyperbaric conditions, in freely moving rats. Amino acids were analysed by HPLC coupled to fluorimetric detection in order to appreciate glutamate, aspartate, glutamine and asparagine levels. Nitrogen–oxygen mixture exposure at 3 MPa decreased glutamate, glutamine and asparagine concentrations. In contrast, with helium–oxygen mixture, glutamate and aspartate levels were increased during the compression phase but not during the stay at maximal pressure. Comparison between nitrogen and helium highlighted the narcotic effects of nitrogen at pressure. As a matter of fact, nitrogen induces a reduction in glutamate and in other amino acids that could partly explain the decrease in striatal dopamine level as well as the motor and cognitive disturbances reported in nitrogen Narcosis.
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TRANSLATIONAL PHYSIOLOGY How can an inert gas counterbalance a NMDA-induced glutamate release?
2009Co-Authors: Nicolas Vallee, Jean-claude Rostain, Jean-jacques RissoAbstract:Previous neurochemical studies performed in rats have revealed a decrease of striatal dopamine and glutamate induced by inert gas Narcosis. We sought to establish the hypothetical role of glutamate and its main receptor, the N-methyl-D-aspartate (NMDA) receptor, in this syndrome. We aimed to counteract the nitrogen Narcosis-induced glutamate and dopamine decreases by stimulating the NMDA receptor in the striatum. We used bilateral retrodialysis on awake rats, submit-ted to nitrogen under pressure (3 MPa). Continuous infusion of 2 mM of NMDA under normobaric conditions (0.01 MPa) (n 8) signifi-cantly increased extracellular average levels of glutamate, aspartate, glutamine, and asparagine by 241.8%, 292.5%, 108.3%, and 195.3%, respectively. The same infusion conducted under nitrogen at 3 MPa (n 6) revealed significant lower levels of these amino acids (n 8/6, P 0.001). In opposition, the NMDA-induced effects on dopa-mine, dihydrophenylacetic acid (DOPAC), and homovanillic aci
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recent neurochemical basis of inert gas Narcosis and pressure effects
Undersea & hyperbaric medicine : journal of the Undersea and Hyperbaric Medical Society, 2006Co-Authors: Jean-claude Rostain, N. BalonAbstract:Compressed air or a nitrogen-oxygen mixture produces from 0.3 MPa nitrogen Narcosis. The traditional view was that anaesthesia or Narcosis occurs when the volume of a hydrophobic site is caused to expand beyond a critical amount by the absorption of molecules of a narcotic gas. The observation of the pressure reversal effect on general anaesthesia has for a long time supported the lipid theory. However, recently, protein theories are in increasing consideration since results have been interpreted as evidence for a direct anaesthetic-protein interaction. The question is to know whether inert gases act by binding processes on proteins of neurotransmitter receptors. Compression with breathing mixtures where nitrogen is replaced by helium which has a low narcotic potency induces from 1 MPa, the high pressure nervous syndrome which is related to neurochemical disturbances including changes of the amino-acid and monoamine neurotransmissions. The use of narcotic gas (nitrogen or hydrogen) added to a helium-oxygen mixture, reduced some symptoms of the HPNS but also had some effects due to an additional effect of the narcotic potency of the gas. The researches performed at the level of basal ganglia of the rat brain and particularly the nigro-striatal pathway involved in the control of the motor, locomotor and cognitive functions, disrupted by Narcosis or pressure, have indicated that GABAergic neurotransmission is implicated via GABAa receptors.
T W Schultz - One of the best experts on this subject based on the ideXlab platform.
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definition of the structural domain of the baseline non polar Narcosis model for tetrahymena pyriformis
Sar and Qsar in Environmental Research, 2008Co-Authors: Claire M Ellison, Judith C Madden, Mark T D Cronin, T W SchultzAbstract:The aim of this work was to develop a high-quality 1-octanol/water partition coefficient-dependent (log P) baseline quantitative structure-activity relationship (QSAR) for the toxicity (log IGC(50)(-1)) of classic non-polar narcotics to Tetrahymena pyriformis, and subsequently use this model to define the domain of applicability for baseline Narcosis. The toxicities to T. pyriformis of 514 possible non-polar narcotics were assessed. A QSAR to predict toxicity was created from a training set of 87 classic non-polar narcotics (the saturated alcohols and ketones): log IGC(50)(-1) = 0.78 log P-2.01 (n = 87, r(2) = 0.96). This model was then used to predict the toxicity of the remaining chemicals. The chemicals from the large dataset which were poorly predicted by the model (i.e. the prediction was > +/-0.5 log units from the experimental value) were used to aid the definition of structural categories of chemicals which are not non-polar narcotics. Doing so has enabled the domain for non-polar Narcosis to be defined in terms of structural categories. Defining domains of applicability for QSAR models is important if they are to be considered for making predictions of toxicity for regulatory purposes.
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definition of the structural domain of the baseline non polar Narcosis model for tetrahymena pyriformis
Sar and Qsar in Environmental Research, 2008Co-Authors: Claire M Ellison, Judith C Madden, Mark T D Cronin, T W SchultzAbstract:The aim of this work was to develop a high-quality 1-octanol/water partition coefficient-dependent (log P) baseline quantitative structure-activity relationship (QSAR) for the toxicity (log ) of classic non-polar narcotics to Tetrahymena pyriformis, and subsequently use this model to define the domain of applicability for baseline Narcosis. The toxicities to T. pyriformis of 514 possible non-polar narcotics were assessed. A QSAR to predict toxicity was created from a training set of 87 classic non-polar narcotics (the saturated alcohols and ketones): log = 0.78 log P–2.01 (n = 87, r 2 = 0.96). This model was then used to predict the toxicity of the remaining chemicals. The chemicals from the large dataset which were poorly predicted by the model (i.e. the prediction was > ±0.5 log units from the experimental value) were used to aid the definition of structural categories of chemicals which are not non-polar narcotics. Doing so has enabled the domain for non-polar Narcosis to be defined in terms of structu...
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structure toxicity relationships for benzenes evaluated with tetrahymena pyriformis
Chemical Research in Toxicology, 1999Co-Authors: T W SchultzAbstract:Toxicity data for 200 substituted benzenes tested in the two-day Tetrahymena pyriformis population growth impairment assay representing the neutral Narcosis, polar Narcosis, respiratory uncoupling, and weak and strong electrophilic mechanisms of toxic action were evaluated. A quantitative structure−toxicity model correlating toxic potency [log(IGC50-1)] with hydrophobicity quantified by the 1-octanol/water partition coefficient (log Kow) and electrophilic reactivity quantified by the molecular orbital parameter, maximum superdelocalizability (Smax), was developed. This model [log(IGC50-1) = 0.50(log Kow) + 9.85(Smax) − 3.47; n = 197, r2 = 0.816, s = 0.34, F = 429, Pr > F = 0.0001] allows for the prediction of acute potency without the a priori identification of the mechanism of action. The examination of residuals reveals that neutral narcotics with high volatility (e.g., methyl- and chloro-substituted benzenes) and highly reactive fluoro- and nitro-containing derivatives are fitted poorly. A comparison o...
Benjamin P Oldroyd - One of the best experts on this subject based on the ideXlab platform.
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no evidence that dna methylation is associated with the regulation of fertility in the adult honey bee apis mellifera hymenoptera apidae worker ovary
Australian Journal of Entomology, 2017Co-Authors: Manlika Kilaso, Benjamin P Oldroyd, Nadine C Chapman, Emily J Remnant, Chanpen ChanchaoAbstract:Epigenetic modifications, mediated by DNA methylation, are involved in caste differentiation between queen and worker honey bees, Apis mellifera. This study uses methylation sensitive amplified fragment length polymorphism (MS-AFLP) to investigate whether genome-wide DNA methylation is implicated in the regulation of honey bee worker sterility and whether CO2 Narcosis, which suppresses ovary activation in queenless workers, influences DNA methylation. Queenless workers were divided into control and experimental (CO2 Narcosis) cages. We compared MS-AFLP patterns in CO2-treated and non-treated workers with and without activated ovaries at 4 h, 2 and 7 days after treatment. While there was evidence of DNA methylation in all samples, there was no detectable difference in genome-wide methylation patterns between any treatment comparisons. This suggests that mechanisms that regulate worker sterility in the adult honey bee worker are not related to genome-wide methylation, and that CO2 Narcosis does not significantly affect DNA methylation patterns in the worker ovary. However, because DNA methylation is sparse in the honey bee, and because MS-AFLP detects only a proportion of methylated sites, it remains possible that a subset of genes that are responsible for the regulation of worker sterility are differentially methylated, but that we failed to pick these up in our genome-wide scan.
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Effects of natural mating and CO2 Narcosis on biogenic amine receptor gene expression in the ovaries and brain of queen honey bees, Apis mellifera.
Insect Molecular Biology, 2012Co-Authors: Vanina Vergoz, Michael Duncan, Julianne Lim, Guénaël Cabanes, Benjamin P OldroydAbstract:A queen honey bee mates at ~6 days of age, storing the sperm in her spermatheca for life. Mating is associated with profound changes in the behaviour and physiology of the queen but the mechanisms underlying these changes are poorly understood. What is known is that the presence of semen in the oviducts and spermatheca is insufficient to initiate laying, and that copulation or CO2 Narcosis is necessary for ovary activation. In this study we use real-time quantitative PCR to investigate the expression of biogenic amine receptor genes in the brain and ovarian tissue of queens in relation to their reproductive status. We show that dopamine, octopamine and serotonin receptor genes are expressed in the ovaries of queens, and that natural mating, CO2 Narcosis, and the presence of semen in the spermatheca differentially affect their expression. We suggest that these changes may be central to the hormonal cascades that are necessary to initiate oogenesis.
Joop L M Hermens - One of the best experts on this subject based on the ideXlab platform.
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Narcosis and chemical reactivity qsars for acute fish toxicity
Quantitative Structure-activity Relationships, 2000Co-Authors: Andreas P Freidig, Joop L M HermensAbstract:Quantitative structure activity relationships (QSAR) that describe the acute fish toxicity have been published for many different groups of reactive organic chemicals. The structural similarity of chemicals within such groups, suggests that they share a common mode of action (MOA) which is based on their common chemical reactivity. Often, however, a descriptor for this reactivity alone can not explain the observed toxicity satisfactory but addition of a hydrophobicity parameter, like log KOW, is found to improve the relationship. In the present paper, an alternative strategy is proposed and tested with three different literature data sets. Instead of searching for better descriptors to establish a QSAR for the whole data set, the assumption that all compounds within the set act by the same MOA was critically reviewed. We tested the hypothesis that some of the compounds within the data sets acted by Narcosis (general anesthesia), a second plausible mode of action in acute fish toxicity. Narcosis potency at observed lethal exposure levels was modeled with a baseline toxicity QSAR. The literature data sets were split in a Narcosis and a reactive subset and for each of them a separate, one-parameter QSAR was established. For a set of OP-esters, nine out of 20 compounds were identified as possible narcotic compounds and their toxicity could be described with a Narcosis QSAR. For the 11 compounds remaining in the reactive subset, a good correlation between acute toxicity and measured, in-vitro AChE inhibition rate was found (r2=0.68) which would have been overlooked if the whole data set was used. The use of two separate QSARs instead of one mixed QSAR was also tested for literature data sets of nitrobenzenes and α,β-unsaturated carboxylates. It was shown that for the description of toxicity data of all three groups of reactive compounds, a model which uses two separate modes of action was superior to a mixed model which uses a reactivity and a hydrophobicity parameter in a multiple linear regression.
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comparing the potency of chemicals with multiple modes of action in aquatic toxicology acute toxicity due to Narcosis versus reactive toxicity of acrylic compounds
Environmental Science & Technology, 1999Co-Authors: Andreas P Freidig, Henk J M Verhaar, Joop L M HermensAbstract:A series of acrylates and methacrylates was used to illustrate a strategy to compare the importance of two modes of action (MOA) and thereby identify the predominant cause of acute fish toxicity. Acrylic compounds are known to be Michael acceptors and may therefore react with glutathione (GSH), causing GSH-depletion in vivo (reactive mechanism). On the other hand, acrylates may also act by a nonspecific mechanism (Narcosis). The following two, physiologically meaningful parameters were calculated in order to estimate the contribution of these two mechanisms to the overall acute toxicity: (i) a lipid normalized body burden for Narcosis and (ii) the potential degree of GSH depletion by chemical reactivity. The degree of GSH depletion was found to be related to the product of the reactivity toward GSH and the exposure concentration. This model was validated with four model compounds and an in vivo study. For both MOA, toxic ratios were calculated and compared for all chemicals in the series. The approach en...
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an lc50 vs time model for the aquatic toxicity of reactive and receptor mediated compounds consequences for bioconcentration kinetics and risk assessment
Environmental Science & Technology, 1999Co-Authors: Henk J M Verhaar, Watze De Wolf, Scott D Dyer, Karin C H M Legierse, Willem Seinen, Joop L M HermensAbstract:For aquatic toxicants that act by so-called nonpolar Narcosis, it is generally acknowledged that the Critical Body Residue (CBR) at death, as a surrogate dose metric for the amount of target that has interacted with the toxicant, is constant. This constancy is not only maintained across exposure times but also across different (Narcosis) compounds as well as species. We present here an alternative model, applicable to reactive and receptor-mediated toxicants, that implies that for these compounds there is no constant CBR. The model also shows that for each single species-compound combination, the Critical Area Under the Curve (CAUC) is constant and independent of exposure time. These findings can have profound consequences for the interpretation of experimental toxicity data (such as 96 h LC50 values) in risk assessment. Among other things, it shows us that for compounds other than nonpolar narcotics, LC50 vs time values may decrease significantly even after bioconcentration steady state has been achieved...
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acute toxicity of nonpolar versus polar Narcosis is there a difference
Environmental Toxicology and Chemistry, 1998Co-Authors: Wouter H J Vaes, Enaut Urrestarazu Ramos, Henk J M Verhaar, Joop L M HermensAbstract:Narcosis I and II chemicals exhibit different lethal body burdens (LBBs) and acute toxicities (median lethal concentrations [LC50's]) in fish, when compared with their log n-octanol-water partition coefficient (K ow ). The higher toxicity of polar Narcosis chemicals has often been suggested to be related to the polar group in these molecules. Recently we showed that membrane (L-α-dimyristoyl phosphatidyl-choline [DMPC])-water partition coefficients (log K DMPC ) are higher than log K ow for Narcosis II chemicals. Using log K DMPC to model the acute toxicities to fish (log LC50) of the two classes of chemicals together, gives one high-quality quantitative structure-activity relationship (R 2 = 0.98, Q 2 = 0.97). In addition, assuming that the apolar fat-water partition coefficient behaves like the n-octanol-water partition coefficient, differences in LBB can also be explained. Thus, using log K DMPC s, all earlier reported quantitative differences between Narcosis I and II chemicals can be explained.
Jean-jacques Risso - One of the best experts on this subject based on the ideXlab platform.
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effects of hyperbaric nitrogen induced Narcosis on response selection processes
Ergonomics, 2014Co-Authors: Cedric Meckler, Jean-jacques Risso, Jeaneric Blatteau, Thierry Hasbroucq, Bruno Schmid, Franck VidalAbstract:Certain underwater circumstances carry risk of inert gas Narcosis. Impairment of sensorimotor information processing due to Narcosis, induced by normobaric nitrous oxide or high partial nitrogen pressure, has been broadly evidenced, by a lengthening of the reaction time (RT). However, the locus of this effect remains a matter of debate. We examined whether inert gas Narcosis affects the response-selection stage of sensorimotor information processing. We compared an air normobaric condition with a hyperbaric condition in which 10 subjects were subjected to 6 absolute atmospheres of 8.33% O2 Nitrox. In both conditions, subjects performed a between-hand choice-RT task in which we explicitly manipulated the stimulus–response association rule. The effect of this manipulation (which is supposed to affect response-selection processes) was modified by inert gas Narcosis. It is concluded, therefore, that response selection processes are among the loci involved in the effect of inert gas Narcosis on information pro...
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Comparison of Nitrogen Narcosis and Helium Pressure Effects on Striatal Amino Acids: A Microdialysis Study in Rats
Neurochemical Research, 2009Co-Authors: Nicolas Vallee, Jean-claude Rostain, Alain Boussuges, Jean-jacques RissoAbstract:Exposure to nitrogen–oxygen mixture at high pressure induces Narcosis, which can be considered as a first step toward general anaesthesia. Narcotic potencies of inert gases are attributed to their lipid solubility. Nitrogen Narcosis induces cognitive and motor disturbances that occur from 0.3 MPa in man and from 1 MPa in rats. Neurochemical studies performed in rats up to 3 MPa have shown that nitrogen pressure decreases striatal dopamine release like argon, another inert gas, or nitrous oxide, an anaesthetic gas. Striatal dopamine release is under glutamatergic and other amino acid neurotransmission regulations. The aim of this work was to study the effects of nitrogen at 3 MPa on striatal amino acid levels and to compare to those of 3 MPa of helium which is not narcotic at this pressure, by using a new technique of microdialysis samples extraction under hyperbaric conditions, in freely moving rats. Amino acids were analysed by HPLC coupled to fluorimetric detection in order to appreciate glutamate, aspartate, glutamine and asparagine levels. Nitrogen–oxygen mixture exposure at 3 MPa decreased glutamate, glutamine and asparagine concentrations. In contrast, with helium–oxygen mixture, glutamate and aspartate levels were increased during the compression phase but not during the stay at maximal pressure. Comparison between nitrogen and helium highlighted the narcotic effects of nitrogen at pressure. As a matter of fact, nitrogen induces a reduction in glutamate and in other amino acids that could partly explain the decrease in striatal dopamine level as well as the motor and cognitive disturbances reported in nitrogen Narcosis.
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TRANSLATIONAL PHYSIOLOGY How can an inert gas counterbalance a NMDA-induced glutamate release?
2009Co-Authors: Nicolas Vallee, Jean-claude Rostain, Jean-jacques RissoAbstract:Previous neurochemical studies performed in rats have revealed a decrease of striatal dopamine and glutamate induced by inert gas Narcosis. We sought to establish the hypothetical role of glutamate and its main receptor, the N-methyl-D-aspartate (NMDA) receptor, in this syndrome. We aimed to counteract the nitrogen Narcosis-induced glutamate and dopamine decreases by stimulating the NMDA receptor in the striatum. We used bilateral retrodialysis on awake rats, submit-ted to nitrogen under pressure (3 MPa). Continuous infusion of 2 mM of NMDA under normobaric conditions (0.01 MPa) (n 8) signifi-cantly increased extracellular average levels of glutamate, aspartate, glutamine, and asparagine by 241.8%, 292.5%, 108.3%, and 195.3%, respectively. The same infusion conducted under nitrogen at 3 MPa (n 6) revealed significant lower levels of these amino acids (n 8/6, P 0.001). In opposition, the NMDA-induced effects on dopa-mine, dihydrophenylacetic acid (DOPAC), and homovanillic aci
