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Jean-jacques Risso - One of the best experts on this subject based on the ideXlab platform.
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Mechanism of Action of Nitrogen Pressure in Controlling Striatal Dopamine Level of Freely Moving Rats is Changed by Recurrent Exposures to Nitrogen Narcosis
Neurochemical Research, 2012Co-Authors: Cécile Lavoute, Jean-jacques Risso, Michel Weiss, Jean-claude RostainAbstract:In rats, a single exposure to 3 MPa Nitrogen induces change in motor processes, a sedative action and a decrease in dopamine release in the striatum. These changes due to a narcotic effect of Nitrogen have been attributed to a decrease in glutamatergic control and the facilitation of GABAergic neurotransmission involving NMDA and GABA_A receptors, respectively. After repeated exposure to Nitrogen Narcosis, a second exposure to 3 MPa increased dopamine levels suggesting a change in the control of the dopaminergic pathway. We investigated the role of the nigral NMDA and GABA_A receptors in changes in the striatal dopamine levels. Dopamine-sensitive electrodes were implanted into the striatum under general anesthesia, together with a guide-cannula for drug injections into the SNc. Dopamine level was monitored by in vivo voltammetry. The effects of NMDA/GABA_A receptor agonists (NMDA/muscimol) and antagonists (AP7/gabazine) on dopamine levels were investigated. Rats were exposed to 3 MPa Nitrogen before and after five daily exposures to 1 MPa. After these exposures to Nitrogen Narcosis, gabazine, NMDA and AP7 had no effect on the Nitrogen-induced increase in dopamine levels. By contrast, muscimol strongly enhanced the increase in dopamine level induced by Nitrogen. Our findings suggest that repeated Nitrogen exposure disrupted NMDA receptor function and decreased GABAergic input by modifying GABA_A receptor sensitivity. These findings demonstrated a change in the mechanism of action of Nitrogen at pressure.
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A Pressurized Nitrogen Counterbalance to Cortical Glutamatergic Pathway Stimulation
Neurochemical Research, 2010Co-Authors: Nicolas Vallee, Jean-claude Rostain, Jean-jacques RissoAbstract:Previous microdialysis studies performed in rats have revealed a decrease of striatal dopamine and glutamate induced by Nitrogen Narcosis. We sought to establish the hypothetical role of the glutamatergic corticostriatal pathway because of the glutamate deficiency which occurs in the basal ganglia in this hyperbaric syndrome. Retrodialysis with 1 mM of Saclofen and 100 mM of KCl in the prefrontal cortex under normobaric conditions led to an increase in striatal levels of glutamate by 95.2% and no changes in dopamine levels. Under 3 MPa of Nitrogen and with the infusion, the rate of striatal glutamate decreased by 51.3%, to a greater extent than under pressurised Nitrogen alone (−23.8%). The rate of dopamine decreased, which also occurred under pressurised Nitrogen (−36.9 and −31.4%, respectively). In conclusion, the function of the corticostriatal pathway is affected by Nitrogen under pressure. This suggests that the Nitrogen-induced break point seems to be located at the glutamatergic striatopetal neurons.
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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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Low susceptibility to inert gases and pressure symptoms in TREK-1-deficient mice.
Neuroreport, 2009Co-Authors: Nicolas Vallee, Jean-claude Rostain, Jean-jacques RissoAbstract:Nervous disorders may occur after an organism is saturated with inert gases, which may alter the lipid bilayer structure, according to their liposolubility coefficient. Increase in the Nitrogen partial pressure induces a neurological syndrome called 'Nitrogen Narcosis'. By contrast, high pressures of helium induce epilepsy, an high-pressure nervous syndrome symptom. On the basis of an analogy with anaesthetic mechanisms, we used TREK-1 knockout mice, earlier described to volatile the anaesthetics resistance. These mice had a higher threshold of resistance to the narcotic effects of Nitrogen and to the death after recurrent epileptic seizure induced by high pressure. TREK-1 channels seem to play a key role in modulating the anaesthetic potential of inert gases and in neuroprotection.
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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
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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Comprehensive Physiology - 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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Mechanism of Action of Nitrogen Pressure in Controlling Striatal Dopamine Level of Freely Moving Rats is Changed by Recurrent Exposures to Nitrogen Narcosis
Neurochemical Research, 2012Co-Authors: Cécile Lavoute, Jean-jacques Risso, Michel Weiss, Jean-claude RostainAbstract:In rats, a single exposure to 3 MPa Nitrogen induces change in motor processes, a sedative action and a decrease in dopamine release in the striatum. These changes due to a narcotic effect of Nitrogen have been attributed to a decrease in glutamatergic control and the facilitation of GABAergic neurotransmission involving NMDA and GABA_A receptors, respectively. After repeated exposure to Nitrogen Narcosis, a second exposure to 3 MPa increased dopamine levels suggesting a change in the control of the dopaminergic pathway. We investigated the role of the nigral NMDA and GABA_A receptors in changes in the striatal dopamine levels. Dopamine-sensitive electrodes were implanted into the striatum under general anesthesia, together with a guide-cannula for drug injections into the SNc. Dopamine level was monitored by in vivo voltammetry. The effects of NMDA/GABA_A receptor agonists (NMDA/muscimol) and antagonists (AP7/gabazine) on dopamine levels were investigated. Rats were exposed to 3 MPa Nitrogen before and after five daily exposures to 1 MPa. After these exposures to Nitrogen Narcosis, gabazine, NMDA and AP7 had no effect on the Nitrogen-induced increase in dopamine levels. By contrast, muscimol strongly enhanced the increase in dopamine level induced by Nitrogen. Our findings suggest that repeated Nitrogen exposure disrupted NMDA receptor function and decreased GABAergic input by modifying GABA_A receptor sensitivity. These findings demonstrated a change in the mechanism of action of Nitrogen at pressure.
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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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A Pressurized Nitrogen Counterbalance to Cortical Glutamatergic Pathway Stimulation
Neurochemical Research, 2010Co-Authors: Nicolas Vallee, Jean-claude Rostain, Jean-jacques RissoAbstract:Previous microdialysis studies performed in rats have revealed a decrease of striatal dopamine and glutamate induced by Nitrogen Narcosis. We sought to establish the hypothetical role of the glutamatergic corticostriatal pathway because of the glutamate deficiency which occurs in the basal ganglia in this hyperbaric syndrome. Retrodialysis with 1 mM of Saclofen and 100 mM of KCl in the prefrontal cortex under normobaric conditions led to an increase in striatal levels of glutamate by 95.2% and no changes in dopamine levels. Under 3 MPa of Nitrogen and with the infusion, the rate of striatal glutamate decreased by 51.3%, to a greater extent than under pressurised Nitrogen alone (−23.8%). The rate of dopamine decreased, which also occurred under pressurised Nitrogen (−36.9 and −31.4%, respectively). In conclusion, the function of the corticostriatal pathway is affected by Nitrogen under pressure. This suggests that the Nitrogen-induced break point seems to be located at the glutamatergic striatopetal neurons.
R A De Blasi - One of the best experts on this subject based on the ideXlab platform.
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inert gas Narcosis in scuba diving different gases different reactions
European Journal of Applied Physiology, 2019Co-Authors: Monica Rocco, Luigi Maggi, Silvia Fiorelli, M Mercieri, P. Benedetto, G. Conte, Costantino Balestra, Paolo Pelaia, R A De BlasiAbstract:Purpose Underwater divers face several potential neurological hazards when breathing compressed gas mixtures including Nitrogen Narcosis which can impact diver’s safety. Various human studies have clearly demonstrated brain impairment due to Nitrogen Narcosis in divers at 4 ATA using critical flicker fusion frequency (CFFF) as a cortical performance indicator. However, recently some authors have proposed a probable adaptive phenomenon during repetitive exposure to high Nitrogen pressure in rats, where they found a reversal effect on dopamine release.
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Inert gas Narcosis in scuba diving, different gases different reactions
European journal of applied physiology, 2018Co-Authors: Monica Rocco, Luigi Maggi, Silvia Fiorelli, M Mercieri, P. Benedetto, G. Conte, Costantino Balestra, Paolo Pelaia, R A De BlasiAbstract:Underwater divers face several potential neurological hazards when breathing compressed gas mixtures including Nitrogen Narcosis which can impact diver’s safety. Various human studies have clearly demonstrated brain impairment due to Nitrogen Narcosis in divers at 4 ATA using critical flicker fusion frequency (CFFF) as a cortical performance indicator. However, recently some authors have proposed a probable adaptive phenomenon during repetitive exposure to high Nitrogen pressure in rats, where they found a reversal effect on dopamine release. Sixty experienced divers breathing Air, Trimix or Heliox, were studied during an open water dive to a depth of 6 ATA with a square profile testing CFFF measurement before (T0), during the dive upon arriving at the bottom (6 ATA) (T1), 20 min of bottom time (T2), and at 5 m (1.5 ATA) (T3). CFFF results showed a slight increase in alertness and arousal during the deep dive regardless of the gas mixture breathed. The percent change in CFFF values at T1 and T2 differed among the three groups being lower in the air group than in the other groups. All CFFF values returned to basal values 5 min before the final ascent at 5 m (T3), but the Trimix measurements were still slightly better than those at T0. Our results highlight that Nitrogen and oxygen alone and in combination can produce neuronal excitability or depression in a dose-related response.
Cécile Lavoute - 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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Comprehensive Physiology - 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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Mechanism of Action of Nitrogen Pressure in Controlling Striatal Dopamine Level of Freely Moving Rats is Changed by Recurrent Exposures to Nitrogen Narcosis
Neurochemical Research, 2012Co-Authors: Cécile Lavoute, Jean-jacques Risso, Michel Weiss, Jean-claude RostainAbstract:In rats, a single exposure to 3 MPa Nitrogen induces change in motor processes, a sedative action and a decrease in dopamine release in the striatum. These changes due to a narcotic effect of Nitrogen have been attributed to a decrease in glutamatergic control and the facilitation of GABAergic neurotransmission involving NMDA and GABA_A receptors, respectively. After repeated exposure to Nitrogen Narcosis, a second exposure to 3 MPa increased dopamine levels suggesting a change in the control of the dopaminergic pathway. We investigated the role of the nigral NMDA and GABA_A receptors in changes in the striatal dopamine levels. Dopamine-sensitive electrodes were implanted into the striatum under general anesthesia, together with a guide-cannula for drug injections into the SNc. Dopamine level was monitored by in vivo voltammetry. The effects of NMDA/GABA_A receptor agonists (NMDA/muscimol) and antagonists (AP7/gabazine) on dopamine levels were investigated. Rats were exposed to 3 MPa Nitrogen before and after five daily exposures to 1 MPa. After these exposures to Nitrogen Narcosis, gabazine, NMDA and AP7 had no effect on the Nitrogen-induced increase in dopamine levels. By contrast, muscimol strongly enhanced the increase in dopamine level induced by Nitrogen. Our findings suggest that repeated Nitrogen exposure disrupted NMDA receptor function and decreased GABAergic input by modifying GABA_A receptor sensitivity. These findings demonstrated a change in the mechanism of action of Nitrogen at pressure.
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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
Nicolas Vallee - One of the best experts on this subject based on the ideXlab platform.
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Effect of an hyperbaric Nitrogen narcotic ambience on arginine and citrulline levels, the precursor and co-product of nitric oxide, in rat striatum
Medical Gas Research, 2011Co-Authors: Nicolas Vallee, Jean-jacques Rissoe, Jean-eric BlatteauAbstract:Previous studies performed in the laboratory have shown that Nitrogen Narcosis induces a decrease in striatal glutamate and dopamine levels. Although we stimulated the N-methyl-D-aspartate (NMDA) receptor, an important glutamate receptor required for motor and locomotor activity managed by the striatum, and demonstrated that the receptor was effective when exposed to Nitrogen at 3MPa, it was not possible to return the striatal glutamate level to its base values. We conclude that it was the striatopetal neurons of the glutamatergic pathways that were mainly affected in this hyperbaric syndrome, without understanding the principal reasons. Hence we sought to establish what happens in the vicinity of the plasma membrane, downstream the NMDA-Receptor, and we used the hypothesis that there could be neuronal nitric oxide synthase (nNOS) disturbances. A microdialysis study was performed in rat striatum in order to analyse levels of citrulline, the NO co-product, and arginine, the NO precursor. Those both NO metabolites were detectable with an HPLC coupled to a fluorimetric detector. Exposure to pressurized Nitrogen induced a reduction in citrulline (-18.9%) and arginine (-10.4%) levels. Under the control normobaric conditions, the striatal NMDA infusion enhanced the citrulline level (+85.6%), whereas under 3 MPa of Nitrogen, the same NMDA infusion did not change the citrulline level which remains equivalent to that of the baseline. The level of arginine increased (+45.7%) under normobaric conditions but a decrease occurred in pressurized Nitrogen (-51.6%). Retrodialysis with Saclofen and KCl in the prefrontal cortex under normobaric conditions led to an increase in striatal levels of citrulline (+30.5%) and a decrease in arginine levels (-67.4%). There was no significant difference when Nitrogen at 3MPa was added. To conclude, the synthesis of citrulline/NO is reduced in Nitrogen Narcosis while it seems possible to activate it artificially by infusion. We have suggested that the low glutamate levels recorded in Nitrogen Narcosis induced these dopamine and NO reductions in the striatum.
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A Pressurized Nitrogen Counterbalance to Cortical Glutamatergic Pathway Stimulation
Neurochemical Research, 2010Co-Authors: Nicolas Vallee, Jean-claude Rostain, Jean-jacques RissoAbstract:Previous microdialysis studies performed in rats have revealed a decrease of striatal dopamine and glutamate induced by Nitrogen Narcosis. We sought to establish the hypothetical role of the glutamatergic corticostriatal pathway because of the glutamate deficiency which occurs in the basal ganglia in this hyperbaric syndrome. Retrodialysis with 1 mM of Saclofen and 100 mM of KCl in the prefrontal cortex under normobaric conditions led to an increase in striatal levels of glutamate by 95.2% and no changes in dopamine levels. Under 3 MPa of Nitrogen and with the infusion, the rate of striatal glutamate decreased by 51.3%, to a greater extent than under pressurised Nitrogen alone (−23.8%). The rate of dopamine decreased, which also occurred under pressurised Nitrogen (−36.9 and −31.4%, respectively). In conclusion, the function of the corticostriatal pathway is affected by Nitrogen under pressure. This suggests that the Nitrogen-induced break point seems to be located at the glutamatergic striatopetal neurons.
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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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Low susceptibility to inert gases and pressure symptoms in TREK-1-deficient mice.
Neuroreport, 2009Co-Authors: Nicolas Vallee, Jean-claude Rostain, Jean-jacques RissoAbstract:Nervous disorders may occur after an organism is saturated with inert gases, which may alter the lipid bilayer structure, according to their liposolubility coefficient. Increase in the Nitrogen partial pressure induces a neurological syndrome called 'Nitrogen Narcosis'. By contrast, high pressures of helium induce epilepsy, an high-pressure nervous syndrome symptom. On the basis of an analogy with anaesthetic mechanisms, we used TREK-1 knockout mice, earlier described to volatile the anaesthetics resistance. These mice had a higher threshold of resistance to the narcotic effects of Nitrogen and to the death after recurrent epileptic seizure induced by high pressure. TREK-1 channels seem to play a key role in modulating the anaesthetic potential of inert gases and in neuroprotection.
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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