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M. S. Bruno - One of the best experts on this subject based on the ideXlab platform.
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gabaergic neurotransmission in the c57bl 10 sps sps Mouse Mutant a model of absence seizures
Experimental Neurology, 1991Co-Authors: J G Ortiz, Arnaldo E. Negrón, A.p. Thomas, H. Heimer, J. A. Moreira, Mayra L. Cordero, J. Aranda, M. S. BrunoAbstract:Abstract The C57BL 10 , sps sps Mouse Mutant displays generalized absence seizure-like behavior. In these mice, glutamic acid decarboxylase activity is reduced in the cortex and hippocampus. Tritiated flunitrazepam binding (3H-flu) is reduced in these areas, as well as in midbrain, cerebellum, and pons-medulla. Quantitative [3H]-flunitrazepam binding autoradiography confirms these observations. GABA uptake by synaptosomes from sps sps mice is also reduced in all the areas studied. Potassium-stimulated, Ca2+-dependent release of radioactivity from synaptosomes preloaded with [14C]-GABA is reduced in the hippocampus, increased in midbrain and pons-medulla, but remains unaltered in the cortex. These results suggest region-specific alterations in GABAergic neurotransmission that may be responsible for the absence-like seizures in C57BL 10 , sps sps mice.
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GABAergic neurotransmission in the C57BL/10 sps/sps Mouse Mutant: a model of absence seizures.
Experimental neurology, 1991Co-Authors: Arnaldo E. Negrón, A.p. Thomas, H. Heimer, J. A. Moreira, Mayra L. Cordero, J. Aranda, M. S. BrunoAbstract:Abstract The C57BL 10 , sps sps Mouse Mutant displays generalized absence seizure-like behavior. In these mice, glutamic acid decarboxylase activity is reduced in the cortex and hippocampus. Tritiated flunitrazepam binding (3H-flu) is reduced in these areas, as well as in midbrain, cerebellum, and pons-medulla. Quantitative [3H]-flunitrazepam binding autoradiography confirms these observations. GABA uptake by synaptosomes from sps sps mice is also reduced in all the areas studied. Potassium-stimulated, Ca2+-dependent release of radioactivity from synaptosomes preloaded with [14C]-GABA is reduced in the hippocampus, increased in midbrain and pons-medulla, but remains unaltered in the cortex. These results suggest region-specific alterations in GABAergic neurotransmission that may be responsible for the absence-like seizures in C57BL 10 , sps sps mice.
Arnaldo E. Negrón - One of the best experts on this subject based on the ideXlab platform.
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gabaergic neurotransmission in the c57bl 10 sps sps Mouse Mutant a model of absence seizures
Experimental Neurology, 1991Co-Authors: J G Ortiz, Arnaldo E. Negrón, A.p. Thomas, H. Heimer, J. A. Moreira, Mayra L. Cordero, J. Aranda, M. S. BrunoAbstract:Abstract The C57BL 10 , sps sps Mouse Mutant displays generalized absence seizure-like behavior. In these mice, glutamic acid decarboxylase activity is reduced in the cortex and hippocampus. Tritiated flunitrazepam binding (3H-flu) is reduced in these areas, as well as in midbrain, cerebellum, and pons-medulla. Quantitative [3H]-flunitrazepam binding autoradiography confirms these observations. GABA uptake by synaptosomes from sps sps mice is also reduced in all the areas studied. Potassium-stimulated, Ca2+-dependent release of radioactivity from synaptosomes preloaded with [14C]-GABA is reduced in the hippocampus, increased in midbrain and pons-medulla, but remains unaltered in the cortex. These results suggest region-specific alterations in GABAergic neurotransmission that may be responsible for the absence-like seizures in C57BL 10 , sps sps mice.
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GABAergic neurotransmission in the C57BL/10 sps/sps Mouse Mutant: a model of absence seizures.
Experimental neurology, 1991Co-Authors: Arnaldo E. Negrón, A.p. Thomas, H. Heimer, J. A. Moreira, Mayra L. Cordero, J. Aranda, M. S. BrunoAbstract:Abstract The C57BL 10 , sps sps Mouse Mutant displays generalized absence seizure-like behavior. In these mice, glutamic acid decarboxylase activity is reduced in the cortex and hippocampus. Tritiated flunitrazepam binding (3H-flu) is reduced in these areas, as well as in midbrain, cerebellum, and pons-medulla. Quantitative [3H]-flunitrazepam binding autoradiography confirms these observations. GABA uptake by synaptosomes from sps sps mice is also reduced in all the areas studied. Potassium-stimulated, Ca2+-dependent release of radioactivity from synaptosomes preloaded with [14C]-GABA is reduced in the hippocampus, increased in midbrain and pons-medulla, but remains unaltered in the cortex. These results suggest region-specific alterations in GABAergic neurotransmission that may be responsible for the absence-like seizures in C57BL 10 , sps sps mice.
Clifford J Rosen - One of the best experts on this subject based on the ideXlab platform.
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Spontaneous fractures in the Mouse Mutant sfx are caused by deletion of the gulonolactone oxidase gene, causing vitamin C deficiency.
Journal of Bone and Mineral Research, 2005Co-Authors: Subburaman Mohan, Anil Kapoor, Anny Singgih, Zhang Zhang, Tim Taylor, Robert B Chadwick, Yoon‐suk Chung, Leah Rae Donahue, Clifford J RosenAbstract:Using a Mouse Mutant that fractures spontaneously and dies at a very young age, we identified that a deletion of the GULO gene, which is involved in the synthesis of vitamin C, is the cause of impaired osteoblast differentiation, reduced bone formation, and development of spontaneous fractures. Introduction: A major public health problem worldwide, osteoporosis is a disease characterized by inadequate bone mass necessary for mechanical support, resulting in bone fracture. To identify the genetic basis for osteoporotic fractures, we used a Mouse model that develops spontaneous fractures (sfx) at a very early age. Materials and Methods: Skeletal phenotype of the sfx phenotype was evaluated by DXA using PIXImus instrumentation and by dynamic histomorphometry. The sfx gene was identified using various molecular genetic approaches, including fine mapping and sequencing of candidate genes, whole genome microarray, and PCR amplification of candidate genes using cDNA and genomic DNA as templates. Gene expression of selected candidate genes was performed using real-time PCR analysis. Osteoblast differentiation was measured by bone marrow stromal cell nodule assay. Results: Femur and tibial BMD were reduced by 27% and 36%, respectively, in sfx mice at 5 weeks of age. Histomorphometric analyses of bones from sfx mice revealed that bone formation rate is reduced by >90% and is caused by impairment of differentiated functions of osteoblasts. The sfx gene was fine mapped to a 2 MB region containing ∼30 genes in chromosome 14. By using various molecular genetic approaches, we identified that deletion of the gulonolactone oxidase (GULO) gene, which is involved in the synthesis of ascorbic acid, is responsible for the sfx phenotype. We established that ascorbic acid deficiency caused by deletion of the GULO gene (38,146-bp region) contributes to fractures and premature death because the sfx phenotype can be corrected in vivo by treating sfx mice with ascorbic acid and because osteoblasts derived from sfx mice are only able to form mineralized nodules when treated with ascorbic acid. Treatment of bone marrow stromal cells derived from sfx/sfx mice in vitro with ascorbic acid increased expression levels of type I collagen, alkaline phosphatase, and osteocalcin several-fold. Conclusion: The sfx is a mutation of the GULO gene, which leads to ascorbic acid deficiency, impaired osteoblast cell function, and fractures in affected mice. Based on these and other findings, we propose that ascorbic acid is essential for the maintenance of differentiated functions of osteoblasts and other cell types.
Mayra L. Cordero - One of the best experts on this subject based on the ideXlab platform.
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gabaergic neurotransmission in the c57bl 10 sps sps Mouse Mutant a model of absence seizures
Experimental Neurology, 1991Co-Authors: J G Ortiz, Arnaldo E. Negrón, A.p. Thomas, H. Heimer, J. A. Moreira, Mayra L. Cordero, J. Aranda, M. S. BrunoAbstract:Abstract The C57BL 10 , sps sps Mouse Mutant displays generalized absence seizure-like behavior. In these mice, glutamic acid decarboxylase activity is reduced in the cortex and hippocampus. Tritiated flunitrazepam binding (3H-flu) is reduced in these areas, as well as in midbrain, cerebellum, and pons-medulla. Quantitative [3H]-flunitrazepam binding autoradiography confirms these observations. GABA uptake by synaptosomes from sps sps mice is also reduced in all the areas studied. Potassium-stimulated, Ca2+-dependent release of radioactivity from synaptosomes preloaded with [14C]-GABA is reduced in the hippocampus, increased in midbrain and pons-medulla, but remains unaltered in the cortex. These results suggest region-specific alterations in GABAergic neurotransmission that may be responsible for the absence-like seizures in C57BL 10 , sps sps mice.
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GABAergic neurotransmission in the C57BL/10 sps/sps Mouse Mutant: a model of absence seizures.
Experimental neurology, 1991Co-Authors: Arnaldo E. Negrón, A.p. Thomas, H. Heimer, J. A. Moreira, Mayra L. Cordero, J. Aranda, M. S. BrunoAbstract:Abstract The C57BL 10 , sps sps Mouse Mutant displays generalized absence seizure-like behavior. In these mice, glutamic acid decarboxylase activity is reduced in the cortex and hippocampus. Tritiated flunitrazepam binding (3H-flu) is reduced in these areas, as well as in midbrain, cerebellum, and pons-medulla. Quantitative [3H]-flunitrazepam binding autoradiography confirms these observations. GABA uptake by synaptosomes from sps sps mice is also reduced in all the areas studied. Potassium-stimulated, Ca2+-dependent release of radioactivity from synaptosomes preloaded with [14C]-GABA is reduced in the hippocampus, increased in midbrain and pons-medulla, but remains unaltered in the cortex. These results suggest region-specific alterations in GABAergic neurotransmission that may be responsible for the absence-like seizures in C57BL 10 , sps sps mice.
J. Aranda - One of the best experts on this subject based on the ideXlab platform.
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gabaergic neurotransmission in the c57bl 10 sps sps Mouse Mutant a model of absence seizures
Experimental Neurology, 1991Co-Authors: J G Ortiz, Arnaldo E. Negrón, A.p. Thomas, H. Heimer, J. A. Moreira, Mayra L. Cordero, J. Aranda, M. S. BrunoAbstract:Abstract The C57BL 10 , sps sps Mouse Mutant displays generalized absence seizure-like behavior. In these mice, glutamic acid decarboxylase activity is reduced in the cortex and hippocampus. Tritiated flunitrazepam binding (3H-flu) is reduced in these areas, as well as in midbrain, cerebellum, and pons-medulla. Quantitative [3H]-flunitrazepam binding autoradiography confirms these observations. GABA uptake by synaptosomes from sps sps mice is also reduced in all the areas studied. Potassium-stimulated, Ca2+-dependent release of radioactivity from synaptosomes preloaded with [14C]-GABA is reduced in the hippocampus, increased in midbrain and pons-medulla, but remains unaltered in the cortex. These results suggest region-specific alterations in GABAergic neurotransmission that may be responsible for the absence-like seizures in C57BL 10 , sps sps mice.
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GABAergic neurotransmission in the C57BL/10 sps/sps Mouse Mutant: a model of absence seizures.
Experimental neurology, 1991Co-Authors: Arnaldo E. Negrón, A.p. Thomas, H. Heimer, J. A. Moreira, Mayra L. Cordero, J. Aranda, M. S. BrunoAbstract:Abstract The C57BL 10 , sps sps Mouse Mutant displays generalized absence seizure-like behavior. In these mice, glutamic acid decarboxylase activity is reduced in the cortex and hippocampus. Tritiated flunitrazepam binding (3H-flu) is reduced in these areas, as well as in midbrain, cerebellum, and pons-medulla. Quantitative [3H]-flunitrazepam binding autoradiography confirms these observations. GABA uptake by synaptosomes from sps sps mice is also reduced in all the areas studied. Potassium-stimulated, Ca2+-dependent release of radioactivity from synaptosomes preloaded with [14C]-GABA is reduced in the hippocampus, increased in midbrain and pons-medulla, but remains unaltered in the cortex. These results suggest region-specific alterations in GABAergic neurotransmission that may be responsible for the absence-like seizures in C57BL 10 , sps sps mice.