The Experts below are selected from a list of 2484 Experts worldwide ranked by ideXlab platform
Jan Albrecht - One of the best experts on this subject based on the ideXlab platform.
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Taurine prevents ammonia-induced accumulation of cyclic GMP in rat striatum by interaction with GABAA and Glycine Receptors.
Brain research, 2005Co-Authors: Wojciech Hilgier, Simo S Oja, Pirjo Saransaari, Jan AlbrechtAbstract:Previously, we had shown that ammonium chloride (ammonia)-induced accumulation of cyclic GMP in the microdialysates of rat striatum is blocked by taurine. In this study, coinfusion with taurine of a GABAA Receptor Antagonist bicuculline or a Glycine Receptor Antagonist strychnine (100 microM each), separately, restored ammonia-induced release of cGMP to the extracellular fluid to approximately 29% and 18% of the level measured in the absence of taurine, respectively. Simultaneous coinfusion of both Antagonists or of 100 muM picrotoxin, which is an Antagonist of both GABAA and Gly Receptors, offsets most of the taurine block. Ammonia-induced accumulation of cyclic GMP was attenuated by approximately 12% upon coinfusion of a GABAA Receptor agonist muscimol (100 microM). The results suggest that stimulation of both GABAA and Glycine Receptors is involved in the mechanism by which taurine limits the activation of the NMDA/NO/cGMP pathway by ammonia in the striatum.
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Taurine prevents ammonia-induced accumulation of cyclic GMP in rat striatum by interaction with GABAA and Glycine Receptors.
Brain Research, 2005Co-Authors: Wojciech Hilgier, Simo S Oja, Pirjo Saransaari, Jan AlbrechtAbstract:Abstract Previously, we had shown that ammonium chloride (ammonia)-induced accumulation of cyclic GMP in the microdialysates of rat striatum is blocked by taurine. In this study, coinfusion with taurine of a GABAA Receptor Antagonist bicuculline or a Glycine Receptor Antagonist strychnine (100 μM each), separately, restored ammonia-induced release of cGMP to the extracellular fluid to ∼29% and 18% of the level measured in the absence of taurine, respectively. Simultaneous coinfusion of both Antagonists or of 100 μM picrotoxin, which is an Antagonist of both GABAA and Gly Receptors, offsets most of the taurine block. Ammonia-induced accumulation of cyclic GMP was attenuated by ∼12% upon coinfusion of a GABAA Receptor agonist muscimol (100 μM). The results suggest that stimulation of both GABAA and Glycine Receptors is involved in the mechanism by which taurine limits the activation of the NMDA/NO/cGMP pathway by ammonia in the striatum.
Wojciech Hilgier - One of the best experts on this subject based on the ideXlab platform.
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Taurine prevents ammonia-induced accumulation of cyclic GMP in rat striatum by interaction with GABAA and Glycine Receptors.
Brain research, 2005Co-Authors: Wojciech Hilgier, Simo S Oja, Pirjo Saransaari, Jan AlbrechtAbstract:Previously, we had shown that ammonium chloride (ammonia)-induced accumulation of cyclic GMP in the microdialysates of rat striatum is blocked by taurine. In this study, coinfusion with taurine of a GABAA Receptor Antagonist bicuculline or a Glycine Receptor Antagonist strychnine (100 microM each), separately, restored ammonia-induced release of cGMP to the extracellular fluid to approximately 29% and 18% of the level measured in the absence of taurine, respectively. Simultaneous coinfusion of both Antagonists or of 100 muM picrotoxin, which is an Antagonist of both GABAA and Gly Receptors, offsets most of the taurine block. Ammonia-induced accumulation of cyclic GMP was attenuated by approximately 12% upon coinfusion of a GABAA Receptor agonist muscimol (100 microM). The results suggest that stimulation of both GABAA and Glycine Receptors is involved in the mechanism by which taurine limits the activation of the NMDA/NO/cGMP pathway by ammonia in the striatum.
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Taurine prevents ammonia-induced accumulation of cyclic GMP in rat striatum by interaction with GABAA and Glycine Receptors.
Brain Research, 2005Co-Authors: Wojciech Hilgier, Simo S Oja, Pirjo Saransaari, Jan AlbrechtAbstract:Abstract Previously, we had shown that ammonium chloride (ammonia)-induced accumulation of cyclic GMP in the microdialysates of rat striatum is blocked by taurine. In this study, coinfusion with taurine of a GABAA Receptor Antagonist bicuculline or a Glycine Receptor Antagonist strychnine (100 μM each), separately, restored ammonia-induced release of cGMP to the extracellular fluid to ∼29% and 18% of the level measured in the absence of taurine, respectively. Simultaneous coinfusion of both Antagonists or of 100 μM picrotoxin, which is an Antagonist of both GABAA and Gly Receptors, offsets most of the taurine block. Ammonia-induced accumulation of cyclic GMP was attenuated by ∼12% upon coinfusion of a GABAA Receptor agonist muscimol (100 μM). The results suggest that stimulation of both GABAA and Glycine Receptors is involved in the mechanism by which taurine limits the activation of the NMDA/NO/cGMP pathway by ammonia in the striatum.
Sture Liljequist - One of the best experts on this subject based on the ideXlab platform.
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Site-specific NMDA Receptor Antagonists produce differential effects on cocaine self-administration in rats.
European Journal of Pharmacology, 1999Co-Authors: Petri Hyytiä, Pia Bäckström, Sture LiljequistAbstract:The effects of site-specific NMDA Receptor Antagonists on intravenous cocaine self-administration were examined in rats trained to self-administer cocaine (0.25 mg/infusion) on a fixed ratio (FR) 5 schedule with a 20-s time-out (TO) after each reinforcer. The non-competitive NMDA Receptor Antagonists, dizocilpine (MK-801, (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine hydrogen maleate) (0.05-0.2 mg/kg i.p.) and memantine (1,3-dimethyl-5-amino-adamantane hydrochloride) (2.5-20 mg/kg i.p.), dose-dependently decreased cocaine self-administration, while the competitive NMDA Receptor Antagonist, CGP 39551 (DL-(E)-2-amino-4-methyl-5-phosphono-3-pentanoic acid carboxyethylester) (2.5-15 mg/kg i.p.), and the NMDA/Glycine Receptor Antagonist, L-701,324 (7-chloro-4-hydroxy-3(3-phenoxy)-phenyl-2(H)quinolone) (1.25-10 mg/kg p.o.), were without effect. Under a progressive ratio (PR) schedule, dizocilpine (0.15 mg/kg i.p.) increased the number of cocaine infusions in a manner similar to increasing the unit dose of cocaine, suggestive of potentiation of cocaine reward. Conversely, memantine (10 mg/kg i.p.) produced rate-decreasing effects on the PR schedule. These results demonstrate that NMDA Receptor Antagonists acting at different modulatory sites of the NMDA Receptor do not share dizocilpine's cocaine reward enhancing effects although they are all known to be effective blockers of NMDA Receptor activity.
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The NMDA/Glycine Receptor Antagonist, L-701,324, produces discriminative stimuli similar to those of ethanol.
European journal of pharmacology, 1997Co-Authors: Jolanta Kotlinska, Sture LiljequistAbstract:The ethanol-like discriminative stimulus properties of a novel NMDA Glycine Receptor Antagonist, L-701,324 ((7-chloro-4-hydroxy-3-(3-phenoxy)phenyl-2-(1H)-quinolone), a polyamine Receptor Antagonist, eliprodil, and a non-competitive NMDA Receptor Antagonist, MK-801 (dizocilpine), were examined in rats trained to discriminate ethanol from vehicle in a two-lever discrimination procedure. In rats trained to discriminate ethanol from vehicle, L-701,324 and MK-801 substituted for ethanol in a dose-dependent fashion with a complete substitution noted following administration of 7.5 mg/kg L-701,324 and 0.2 mg/kg MK-801, respectively. Full substitution for ethanol was achieved with no alteration in the rate of responding. In contrast, administration of eliprodil (in doses up to 5 mg/kg) showed only a partial, but not dose-dependent, substitution for ethanol. These findings indicate that a reduction of NMDA Receptor activity, produced either via a blockade of non-competitive NMDA recognition sites or of NMDA/Glycine-sensitive regulatory sites, had discriminative stimulus properties that are similar to those produced by ethanol. Furthermore, the observation that the NMDA/Glycine Receptor Antagonist, L-701,324, was a more effective substitute for ethanol than was the polyamine Antagonist, eliprodil, suggests that several NMDA Receptor subunits, and thus not only NMDAR2B Receptor subunits, are of importance for the discriminative stimulus effects of ethanol.
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the nmda Glycine Receptor Antagonist l 701 324 produces discriminative stimuli similar to those of ethanol
European Journal of Pharmacology, 1997Co-Authors: Jolanta Kotlinska, Sture LiljequistAbstract:The ethanol-like discriminative stimulus properties of a novel NMDA Glycine Receptor Antagonist, L-701,324 ((7-chloro-4-hydroxy-3-(3-phenoxy)phenyl-2-(1H)-quinolone), a polyamine Receptor Antagonist, eliprodil, and a non-competitive NMDA Receptor Antagonist, MK-801 (dizocilpine), were examined in rats trained to discriminate ethanol from vehicle in a two-lever discrimination procedure. In rats trained to discriminate ethanol from vehicle, L-701,324 and MK-801 substituted for ethanol in a dose-dependent fashion with a complete substitution noted following administration of 7.5 mg/kg L-701,324 and 0.2 mg/kg MK-801, respectively. Full substitution for ethanol was achieved with no alteration in the rate of responding. In contrast, administration of eliprodil (in doses up to 5 mg/kg) showed only a partial, but not dose-dependent, substitution for ethanol. These findings indicate that a reduction of NMDA Receptor activity, produced either via a blockade of non-competitive NMDA recognition sites or of NMDA/Glycine-sensitive regulatory sites, had discriminative stimulus properties that are similar to those produced by ethanol. Furthermore, the observation that the NMDA/Glycine Receptor Antagonist, L-701,324, was a more effective substitute for ethanol than was the polyamine Antagonist, eliprodil, suggests that several NMDA Receptor subunits, and thus not only NMDAR2B Receptor subunits, are of importance for the discriminative stimulus effects of ethanol.
Pirjo Saransaari - One of the best experts on this subject based on the ideXlab platform.
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Taurine prevents ammonia-induced accumulation of cyclic GMP in rat striatum by interaction with GABAA and Glycine Receptors.
Brain research, 2005Co-Authors: Wojciech Hilgier, Simo S Oja, Pirjo Saransaari, Jan AlbrechtAbstract:Previously, we had shown that ammonium chloride (ammonia)-induced accumulation of cyclic GMP in the microdialysates of rat striatum is blocked by taurine. In this study, coinfusion with taurine of a GABAA Receptor Antagonist bicuculline or a Glycine Receptor Antagonist strychnine (100 microM each), separately, restored ammonia-induced release of cGMP to the extracellular fluid to approximately 29% and 18% of the level measured in the absence of taurine, respectively. Simultaneous coinfusion of both Antagonists or of 100 muM picrotoxin, which is an Antagonist of both GABAA and Gly Receptors, offsets most of the taurine block. Ammonia-induced accumulation of cyclic GMP was attenuated by approximately 12% upon coinfusion of a GABAA Receptor agonist muscimol (100 microM). The results suggest that stimulation of both GABAA and Glycine Receptors is involved in the mechanism by which taurine limits the activation of the NMDA/NO/cGMP pathway by ammonia in the striatum.
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Taurine prevents ammonia-induced accumulation of cyclic GMP in rat striatum by interaction with GABAA and Glycine Receptors.
Brain Research, 2005Co-Authors: Wojciech Hilgier, Simo S Oja, Pirjo Saransaari, Jan AlbrechtAbstract:Abstract Previously, we had shown that ammonium chloride (ammonia)-induced accumulation of cyclic GMP in the microdialysates of rat striatum is blocked by taurine. In this study, coinfusion with taurine of a GABAA Receptor Antagonist bicuculline or a Glycine Receptor Antagonist strychnine (100 μM each), separately, restored ammonia-induced release of cGMP to the extracellular fluid to ∼29% and 18% of the level measured in the absence of taurine, respectively. Simultaneous coinfusion of both Antagonists or of 100 μM picrotoxin, which is an Antagonist of both GABAA and Gly Receptors, offsets most of the taurine block. Ammonia-induced accumulation of cyclic GMP was attenuated by ∼12% upon coinfusion of a GABAA Receptor agonist muscimol (100 μM). The results suggest that stimulation of both GABAA and Glycine Receptors is involved in the mechanism by which taurine limits the activation of the NMDA/NO/cGMP pathway by ammonia in the striatum.
Simo S Oja - One of the best experts on this subject based on the ideXlab platform.
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Taurine prevents ammonia-induced accumulation of cyclic GMP in rat striatum by interaction with GABAA and Glycine Receptors.
Brain research, 2005Co-Authors: Wojciech Hilgier, Simo S Oja, Pirjo Saransaari, Jan AlbrechtAbstract:Previously, we had shown that ammonium chloride (ammonia)-induced accumulation of cyclic GMP in the microdialysates of rat striatum is blocked by taurine. In this study, coinfusion with taurine of a GABAA Receptor Antagonist bicuculline or a Glycine Receptor Antagonist strychnine (100 microM each), separately, restored ammonia-induced release of cGMP to the extracellular fluid to approximately 29% and 18% of the level measured in the absence of taurine, respectively. Simultaneous coinfusion of both Antagonists or of 100 muM picrotoxin, which is an Antagonist of both GABAA and Gly Receptors, offsets most of the taurine block. Ammonia-induced accumulation of cyclic GMP was attenuated by approximately 12% upon coinfusion of a GABAA Receptor agonist muscimol (100 microM). The results suggest that stimulation of both GABAA and Glycine Receptors is involved in the mechanism by which taurine limits the activation of the NMDA/NO/cGMP pathway by ammonia in the striatum.
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Taurine prevents ammonia-induced accumulation of cyclic GMP in rat striatum by interaction with GABAA and Glycine Receptors.
Brain Research, 2005Co-Authors: Wojciech Hilgier, Simo S Oja, Pirjo Saransaari, Jan AlbrechtAbstract:Abstract Previously, we had shown that ammonium chloride (ammonia)-induced accumulation of cyclic GMP in the microdialysates of rat striatum is blocked by taurine. In this study, coinfusion with taurine of a GABAA Receptor Antagonist bicuculline or a Glycine Receptor Antagonist strychnine (100 μM each), separately, restored ammonia-induced release of cGMP to the extracellular fluid to ∼29% and 18% of the level measured in the absence of taurine, respectively. Simultaneous coinfusion of both Antagonists or of 100 μM picrotoxin, which is an Antagonist of both GABAA and Gly Receptors, offsets most of the taurine block. Ammonia-induced accumulation of cyclic GMP was attenuated by ∼12% upon coinfusion of a GABAA Receptor agonist muscimol (100 μM). The results suggest that stimulation of both GABAA and Glycine Receptors is involved in the mechanism by which taurine limits the activation of the NMDA/NO/cGMP pathway by ammonia in the striatum.