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Marco Antonio Campana Venditti - One of the best experts on this subject based on the ideXlab platform.
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Rats With Different Thresholds to Clonic Convulsions Induced by DMCM Differ in the Binding of [^3H]-MK-801 and [^3H]-Ouabain in the Membranes of Brain Regions
Neurochemical Research, 2012Co-Authors: Marcos Brandão Contó, José Gilberto Barbosa De Carvalho, Marco Antonio Campana VendittiAbstract:Considering the putative participation of N-methyl-D-aspartate (NMDA) receptors and the Na^+, K^+-ATPase enzymes in the susceptibility to convulsions induced by the benzodiazepine inverse agonist methyl 6,7-dimethoxy-4-ethyl-β-carboline-3-carboxylate (DMCM), the present study sought to determine if rats with high (HTR) and low (LTR) thresholds to clonic convulsions induced by DMCM differed in the following aspects: the binding of NMDA receptors by [^3H]-MK-801, Na^+, K^+-ATPase activity (K^+-stimulated p -nitrophenylphosphatase) and high-affinity [^3H]-ouabain binding to membranes from discrete brain regions. Compared to the HTR subgroup, the LTR subgroup presented a lower binding of [^3H]-MK-801 in the hippocampus, frontal cortex and striatum. The subgroups did not differ in K^+- p -nitrophenylphosphatase activity, but the LTR subgroup had a lower density of isozymes with a high-affinity to ouabain in the brainstem and in the frontal cortex and a lower affinity to ouabain in the hippocampus than the HTR subgroup. These results suggest that NMDA receptors and ouabain-sensitive Na^+, K^+-ATPase isozymes may underlie the susceptibility to DMCM-induced convulsions.
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Rats with different thresholds to clonic convulsions induced by DMCM differ in the binding of [3H]-MK-801 and [3H]-ouabain in the membranes of brain regions.
Neurochemical Research, 2012Co-Authors: Marcos Brandão Contó, José Gilberto Barbosa De Carvalho, Marco Antonio Campana VendittiAbstract:Considering the putative participation of N-methyl-D-aspartate (NMDA) receptors and the Na+, K+-ATPase enzymes in the susceptibility to convulsions induced by the benzodiazepine inverse agonist methyl 6,7-dimethoxy-4-ethyl-β-carboline-3-carboxylate (DMCM), the present study sought to determine if rats with high (HTR) and low (LTR) thresholds to clonic convulsions induced by DMCM differed in the following aspects: the binding of NMDA receptors by [3H]-MK-801, Na+, K+-ATPase activity (K+-stimulated p-nitrophenylphosphatase) and high-affinity [3H]-ouabain binding to membranes from discrete brain regions. Compared to the HTR subgroup, the LTR subgroup presented a lower binding of [3H]-MK-801 in the hippocampus, frontal cortex and striatum. The subgroups did not differ in K+-p-nitrophenylphosphatase activity, but the LTR subgroup had a lower density of isozymes with a high-affinity to ouabain in the brainstem and in the frontal cortex and a lower affinity to ouabain in the hippocampus than the HTR subgroup. These results suggest that NMDA receptors and ouabain-sensitive Na+, K+-ATPase isozymes may underlie the susceptibility to DMCM-induced convulsions.
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Rats with different thresholds for DMCM-induced clonic convulsions differ in the sleep-time of diazepam and [3H]-Ro 15-4513 binding
Epilepsy Research, 2011Co-Authors: Marcos Brandão Contó, José Gilberto Barbosa De Carvalho, Débora C. Hipólide, Marco Antonio Campana VendittiAbstract:Summary The current study investigated the possible inherent relationship between convulsions and sleep involving the GABA A /benzodiazepine site complex. The aim of this study was to determine if rats with high (HTR) and low (LTR) thresholds for clonic convulsions induced by DMCM, a benzodiazepine inverse agonist, differ in the following aspects: (1) sensitivity to the hypnotic effects of the GABA A positive allosteric modulators diazepam, pentobarbital and ethanol and (2) in the binding of [ 3 H]-flunitrazepam, a benzodiazepine agonist, measured by autoradiography, and [ 3 H]-Ro 15-4513, a benzodiazepine partial inverse agonist, to membranes from discrete brain regions. The LTR subgroup presented a shorter diazepam-induced sleeping time compared to that of the HTR subgroup. Biochemical assays revealed that the LTR subgroup did not differ in [ 3 H]-flunitrazepam binding compared to the HTR subgroup. With respect to the binding of [ 3 H]-Ro 15-4513, the LTR subgroup had higher binding in the brainstem and lower binding in the striatum compared to the HTR subgroup. These results suggest that differences in the benzodiazepine site on the GABA A receptor may underlie the susceptibility to DMCM-induced convulsions and sensitivity to the hypnotic effect of diazepam.
Aaron P Russell - One of the best experts on this subject based on the ideXlab platform.
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ucp3 protein regulation in human skeletal muscle fibre types i iia and iix is dependent on exercise intensity
The Journal of Physiology, 2003Co-Authors: Aaron P Russell, Emmanuel Somm, Manu Praz, Antoinette Crettenand, Oliver Hartley, Astrid Melotti, Jean-paul Giacobino, Patrick Muzzin, Charles GobeletAbstract:It has been proposed that mitochondrial uncoupling protein 3 (UCP3) behaves as an uncoupler of oxidative phosphorylation. In a cross-sectional study, UCP3 protein levels were found to be lower in all fibre types of endurance-trained cyclists as compared to healthy controls. This decrease was greatest in the type I oxidative fibres, and it was hypothesised that this may be due to the preferential recruitment of these fibres during endurance training. To test this hypothesis, we compared the effects of 6 weeks of endurance (ETr) and sprint (STr) running training on UCP3 mRNA expression and fibre-type protein content using real-time PCR and immunofluorescence techniques, respectively. UCP3 mRNA and protein levels were downregulated similarly in ETr and STr (UCP3 mRNA: by 65 and 50 %, respectively; protein: by 30 and 27 %, respectively). ETr significantly reduced UCP3 protein content in type I, IIa and IIx muscle fibres by 54, 29 and 16 %, respectively. STr significantly reduced UCP3 protein content in type I, IIa and IIx muscle fibres by 24, 31 and 26 %, respectively. The fibre-type reductions in UCP3 due to ETr, but not STr, were significantly different from each other, with the effect being greater in type I than in type IIa, and in type IIa than in type IIx fibres. As a result, compared to STr, ETr reduced UCP3 expression significantly more in fibre type I and significantly less in fibre types IIx. This suggests that the more a fibre is recruited, the more it adapts to training by a decrease in its UCP3 expression. In addition, the more a fibre type depends on fatty acid β oxidation and oxidative phosphorylation, the more it responds to ETr by a decrease in its UCP3 content.
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UCP3 protein regulation in human skeletal muscle fibre types I, IIa and IIx is dependent on exercise intensity.
The Journal of physiology, 2003Co-Authors: Aaron P Russell, Emmanuel Somm, Manu Praz, Antoinette Crettenand, Oliver Hartley, Astrid Melotti, Jean-paul Giacobino, Patrick Muzzin, Charles Gobelet, Olivier DériazAbstract:It has been proposed that mitochondrial uncoupling protein 3 (UCP3) behaves as an uncoupler of oxidative phosphorylation. In a cross-sectional study, UCP3 protein levels were found to be lower in all fibre types of endurance-trained cyclists as compared to healthy controls. This decrease was greatest in the type I oxidative fibres, and it was hypothesised that this may be due to the preferential recruitment of these fibres during endurance training. To test this hypothesis, we compared the effects of 6 weeks of endurance (ETr) and sprint (STr) running training on UCP3 mRNA expression and fibre-type protein content using real-time PCR and immunofluorescence techniques, respectively. UCP3 mRNA and protein levels were downregulated similarly in ETr and STr (UCP3 mRNA: by 65 and 50%, respectively; protein: by 30 and 27%, respectively). ETr significantly reduced UCP3 protein content in type I, IIa and IIx muscle fibres by 54, 29 and 16%, respectively. STr significantly reduced UCP3 protein content in type I, IIa and IIx muscle fibres by 24, 31 and 26%, respectively. The fibre-type reductions in UCP3 due to ETr, but not STr, were significantly different from each other, with the effect being greater in type I than in type IIa, and in type IIa than in type IIx fibres. As a result, compared to STr, ETr reduced UCP3 expression significantly more in fibre type I and significantly less in fibre types IIx. This suggests that the more a fibre is recruited, the more it adapts to training by a decrease in its UCP3 expression. In addition, the more a fibre type depends on fatty acid beta oxidation and oxidative phosphorylation, the more it responds to ETr by a decrease in its UCP3 content.
Raymond W Nims - One of the best experts on this subject based on the ideXlab platform.
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induction of cytochrome p 450 in sigmodon hispidus cotton rats exposed to dietary aroclor 1254
Journal of Toxicology and Environmental Health, 1994Co-Authors: John R Henneman, Ronald A. Lubet, Jerrold M Ward, Raymond W NimsAbstract:The induction of immunoreactive cytochrome P‐450 protein and associated catalytic activities in 10‐wk‐old male and female Sigmodon hispidus (cotton rats) exposed for 2 wk to low dietary levels of Aroclor 1254 (0.33, 1.0, 3.3, 10, and 33 ppm), or the prototype P‐450 inducers phenobarbital, DDT, clotrimazole, and β‐naphthoflavone was examined. Ethoxy‐(ETR), methoxy‐ (MTR), pentoxy‐ (PTR), and benzyloxyresorufin (BZR) O‐dealkylation activities were significantly increased at 0.33 ppm Aroclor for males and 1.0 ppm for females.
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Induction of cytochrome P‐450 in sigmodon hispidus (cotton rats) exposed to dietary aroclor 1254
Journal of Toxicology and Environmental Health, 1994Co-Authors: John R Henneman, Ronald A. Lubet, Jerrold M Ward, Raymond W NimsAbstract:The induction of immunoreactive cytochrome P‐450 protein and associated catalytic activities in 10‐wk‐old male and female Sigmodon hispidus (cotton rats) exposed for 2 wk to low dietary levels of Aroclor 1254 (0.33, 1.0, 3.3, 10, and 33 ppm), or the prototype P‐450 inducers phenobarbital, DDT, clotrimazole, and β‐naphthoflavone was examined. Ethoxy‐(ETR), methoxy‐ (MTR), pentoxy‐ (PTR), and benzyloxyresorufin (BZR) O‐dealkylation activities were significantly increased at 0.33 ppm Aroclor for males and 1.0 ppm for females.
Marcos Brandão Contó - One of the best experts on this subject based on the ideXlab platform.
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Rats With Different Thresholds to Clonic Convulsions Induced by DMCM Differ in the Binding of [^3H]-MK-801 and [^3H]-Ouabain in the Membranes of Brain Regions
Neurochemical Research, 2012Co-Authors: Marcos Brandão Contó, José Gilberto Barbosa De Carvalho, Marco Antonio Campana VendittiAbstract:Considering the putative participation of N-methyl-D-aspartate (NMDA) receptors and the Na^+, K^+-ATPase enzymes in the susceptibility to convulsions induced by the benzodiazepine inverse agonist methyl 6,7-dimethoxy-4-ethyl-β-carboline-3-carboxylate (DMCM), the present study sought to determine if rats with high (HTR) and low (LTR) thresholds to clonic convulsions induced by DMCM differed in the following aspects: the binding of NMDA receptors by [^3H]-MK-801, Na^+, K^+-ATPase activity (K^+-stimulated p -nitrophenylphosphatase) and high-affinity [^3H]-ouabain binding to membranes from discrete brain regions. Compared to the HTR subgroup, the LTR subgroup presented a lower binding of [^3H]-MK-801 in the hippocampus, frontal cortex and striatum. The subgroups did not differ in K^+- p -nitrophenylphosphatase activity, but the LTR subgroup had a lower density of isozymes with a high-affinity to ouabain in the brainstem and in the frontal cortex and a lower affinity to ouabain in the hippocampus than the HTR subgroup. These results suggest that NMDA receptors and ouabain-sensitive Na^+, K^+-ATPase isozymes may underlie the susceptibility to DMCM-induced convulsions.
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Rats with different thresholds to clonic convulsions induced by DMCM differ in the binding of [3H]-MK-801 and [3H]-ouabain in the membranes of brain regions.
Neurochemical Research, 2012Co-Authors: Marcos Brandão Contó, José Gilberto Barbosa De Carvalho, Marco Antonio Campana VendittiAbstract:Considering the putative participation of N-methyl-D-aspartate (NMDA) receptors and the Na+, K+-ATPase enzymes in the susceptibility to convulsions induced by the benzodiazepine inverse agonist methyl 6,7-dimethoxy-4-ethyl-β-carboline-3-carboxylate (DMCM), the present study sought to determine if rats with high (HTR) and low (LTR) thresholds to clonic convulsions induced by DMCM differed in the following aspects: the binding of NMDA receptors by [3H]-MK-801, Na+, K+-ATPase activity (K+-stimulated p-nitrophenylphosphatase) and high-affinity [3H]-ouabain binding to membranes from discrete brain regions. Compared to the HTR subgroup, the LTR subgroup presented a lower binding of [3H]-MK-801 in the hippocampus, frontal cortex and striatum. The subgroups did not differ in K+-p-nitrophenylphosphatase activity, but the LTR subgroup had a lower density of isozymes with a high-affinity to ouabain in the brainstem and in the frontal cortex and a lower affinity to ouabain in the hippocampus than the HTR subgroup. These results suggest that NMDA receptors and ouabain-sensitive Na+, K+-ATPase isozymes may underlie the susceptibility to DMCM-induced convulsions.
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Rats with different thresholds for DMCM-induced clonic convulsions differ in the sleep-time of diazepam and [3H]-Ro 15-4513 binding
Epilepsy Research, 2011Co-Authors: Marcos Brandão Contó, José Gilberto Barbosa De Carvalho, Débora C. Hipólide, Marco Antonio Campana VendittiAbstract:Summary The current study investigated the possible inherent relationship between convulsions and sleep involving the GABA A /benzodiazepine site complex. The aim of this study was to determine if rats with high (HTR) and low (LTR) thresholds for clonic convulsions induced by DMCM, a benzodiazepine inverse agonist, differ in the following aspects: (1) sensitivity to the hypnotic effects of the GABA A positive allosteric modulators diazepam, pentobarbital and ethanol and (2) in the binding of [ 3 H]-flunitrazepam, a benzodiazepine agonist, measured by autoradiography, and [ 3 H]-Ro 15-4513, a benzodiazepine partial inverse agonist, to membranes from discrete brain regions. The LTR subgroup presented a shorter diazepam-induced sleeping time compared to that of the HTR subgroup. Biochemical assays revealed that the LTR subgroup did not differ in [ 3 H]-flunitrazepam binding compared to the HTR subgroup. With respect to the binding of [ 3 H]-Ro 15-4513, the LTR subgroup had higher binding in the brainstem and lower binding in the striatum compared to the HTR subgroup. These results suggest that differences in the benzodiazepine site on the GABA A receptor may underlie the susceptibility to DMCM-induced convulsions and sensitivity to the hypnotic effect of diazepam.
Charles Gobelet - One of the best experts on this subject based on the ideXlab platform.
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ucp3 protein regulation in human skeletal muscle fibre types i iia and iix is dependent on exercise intensity
The Journal of Physiology, 2003Co-Authors: Aaron P Russell, Emmanuel Somm, Manu Praz, Antoinette Crettenand, Oliver Hartley, Astrid Melotti, Jean-paul Giacobino, Patrick Muzzin, Charles GobeletAbstract:It has been proposed that mitochondrial uncoupling protein 3 (UCP3) behaves as an uncoupler of oxidative phosphorylation. In a cross-sectional study, UCP3 protein levels were found to be lower in all fibre types of endurance-trained cyclists as compared to healthy controls. This decrease was greatest in the type I oxidative fibres, and it was hypothesised that this may be due to the preferential recruitment of these fibres during endurance training. To test this hypothesis, we compared the effects of 6 weeks of endurance (ETr) and sprint (STr) running training on UCP3 mRNA expression and fibre-type protein content using real-time PCR and immunofluorescence techniques, respectively. UCP3 mRNA and protein levels were downregulated similarly in ETr and STr (UCP3 mRNA: by 65 and 50 %, respectively; protein: by 30 and 27 %, respectively). ETr significantly reduced UCP3 protein content in type I, IIa and IIx muscle fibres by 54, 29 and 16 %, respectively. STr significantly reduced UCP3 protein content in type I, IIa and IIx muscle fibres by 24, 31 and 26 %, respectively. The fibre-type reductions in UCP3 due to ETr, but not STr, were significantly different from each other, with the effect being greater in type I than in type IIa, and in type IIa than in type IIx fibres. As a result, compared to STr, ETr reduced UCP3 expression significantly more in fibre type I and significantly less in fibre types IIx. This suggests that the more a fibre is recruited, the more it adapts to training by a decrease in its UCP3 expression. In addition, the more a fibre type depends on fatty acid β oxidation and oxidative phosphorylation, the more it responds to ETr by a decrease in its UCP3 content.
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UCP3 protein regulation in human skeletal muscle fibre types I, IIa and IIx is dependent on exercise intensity.
The Journal of physiology, 2003Co-Authors: Aaron P Russell, Emmanuel Somm, Manu Praz, Antoinette Crettenand, Oliver Hartley, Astrid Melotti, Jean-paul Giacobino, Patrick Muzzin, Charles Gobelet, Olivier DériazAbstract:It has been proposed that mitochondrial uncoupling protein 3 (UCP3) behaves as an uncoupler of oxidative phosphorylation. In a cross-sectional study, UCP3 protein levels were found to be lower in all fibre types of endurance-trained cyclists as compared to healthy controls. This decrease was greatest in the type I oxidative fibres, and it was hypothesised that this may be due to the preferential recruitment of these fibres during endurance training. To test this hypothesis, we compared the effects of 6 weeks of endurance (ETr) and sprint (STr) running training on UCP3 mRNA expression and fibre-type protein content using real-time PCR and immunofluorescence techniques, respectively. UCP3 mRNA and protein levels were downregulated similarly in ETr and STr (UCP3 mRNA: by 65 and 50%, respectively; protein: by 30 and 27%, respectively). ETr significantly reduced UCP3 protein content in type I, IIa and IIx muscle fibres by 54, 29 and 16%, respectively. STr significantly reduced UCP3 protein content in type I, IIa and IIx muscle fibres by 24, 31 and 26%, respectively. The fibre-type reductions in UCP3 due to ETr, but not STr, were significantly different from each other, with the effect being greater in type I than in type IIa, and in type IIa than in type IIx fibres. As a result, compared to STr, ETr reduced UCP3 expression significantly more in fibre type I and significantly less in fibre types IIx. This suggests that the more a fibre is recruited, the more it adapts to training by a decrease in its UCP3 expression. In addition, the more a fibre type depends on fatty acid beta oxidation and oxidative phosphorylation, the more it responds to ETr by a decrease in its UCP3 content.