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article, research, hyperglycemic, content, min, ischemia, rats, atp, privacy, cookies, hippocampus, access, information, publish, search, experimental, brain, state, rat, cell, damage, cyclosporin, subjects, study, glucose, data, log, journal, bioenergetic, folbergrová, uchino, neuronal, animals, ischemic, pcr, glycogen, delayed, products, discover, springer, optional, personal, parties, policy, find, track, prevention, cite, pingan, majlis,

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month download article/chapter experimental brain research experimental research center lps-induced neuroinflammation privacy choices/manage cookies full article pdf glycolytic products 24 prevent cell depolarization bioenergetic state hyperglycemic animals failed hyperglycemic animals displayed delayed neuronal necrosis ischemically preconditioned rats hyperglycemic rats leads rat access european economic area scope submit manuscript maj-lis smith freezing delay considered oxidative stress triggered virtually specific inhibitor maj-lis smith  conditions privacy policy delayed neuronal damage moderate neuronal necrosis extracellular calcium concentration metabolic perturbation observed related subjects accepting optional cookies rat hippocampus journal finder publish 2018 gallic acid article log hyperglycemic subjects check access instant access cell damage hyperglycemic rats article cite recent study present study article folbergrová privacy policy personal data books a dorsal hippocampus optional cookies manage preferences largely maintained transient ischemia

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         headline:Changes in the bioenergetic state of rat hippocampus during 2.5 min of ischemia, and prevention of cell damage by cyclosporin A in hyperglycemic subjects
         description: A recent study from this laboratory has shown that brief transient ischemia (2 min 30 s) in normo- and hyperglycemic rats leads to moderate neuronal necrosis in CA1 cells of the hippocampus, of equal density in the two groups. However, hyperglycemic animals failed to depolarize during the ischemia, nor did they show a decrease in extracellular calcium concentration. The present study was undertaken to study the metabolic correlates to these unexpected findings. Normoglycemic (plasma glucose ∼6 mM) and hyperglycemic (∼20 mM) rats were subjected to ischemic periods of 1 min and 2 min 15 s (2 min 30 s with freezing delay considered), and their brains were frozen in situ. Samples of dorsal hippocampus were dissected at –22°C and extracted for the measurement of phosphocreatine (PCr), creatine, ATP, ADP, AMP, glucose, glycogen, and lactate. Normoglycemic animals showed rapid depletion of PCr, ATP, glucose, and glycogen, and a rise in lactate content to 10–12 mM·kg–1 during the ischemia. Hyperglycemic animals displayed a more moderate rate of fall of PCr and ATP, with ATP values exceeding 50% of control after 2 min 30 s. Glycogen stores were largely maintained, but degradation of glucose somewhat enhanced the lactic acidosis. The results demonstrate that hyperglycemic rats maintained ATP at levels sufficient to prevent cell depolarization and calcium influx during the ischemic period. However, the metabolic perturbation observed must have been responsible for the delayed neuronal damage. We speculate that lowered ATP, increased inorganic P, and oxidative stress triggered a delayed mitochondrial permeability transition (MPT), which led to delayed neuronal necrosis. This assumption was supported by a second series of experiments in which CA1 damage in hyperglycemic rats was prevented by cyclosporin A, a virtually specific inhibitor of the MPT.
         datePublished:
         dateModified:
         pageStart:44
         pageEnd:50
         sameAs:https://doi.org/10.1007/PL00005622
         keywords:
            Key words Forebrain ischemia
            Hyperglycemia
            Hippocampus
            Bioenergetic state
            Cyclosporin A
            Rat
            Neurosciences
            Neurology
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               name:J. Folbergrová
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      headline:Changes in the bioenergetic state of rat hippocampus during 2.5 min of ischemia, and prevention of cell damage by cyclosporin A in hyperglycemic subjects
      description: A recent study from this laboratory has shown that brief transient ischemia (2 min 30 s) in normo- and hyperglycemic rats leads to moderate neuronal necrosis in CA1 cells of the hippocampus, of equal density in the two groups. However, hyperglycemic animals failed to depolarize during the ischemia, nor did they show a decrease in extracellular calcium concentration. The present study was undertaken to study the metabolic correlates to these unexpected findings. Normoglycemic (plasma glucose ∼6 mM) and hyperglycemic (∼20 mM) rats were subjected to ischemic periods of 1 min and 2 min 15 s (2 min 30 s with freezing delay considered), and their brains were frozen in situ. Samples of dorsal hippocampus were dissected at –22°C and extracted for the measurement of phosphocreatine (PCr), creatine, ATP, ADP, AMP, glucose, glycogen, and lactate. Normoglycemic animals showed rapid depletion of PCr, ATP, glucose, and glycogen, and a rise in lactate content to 10–12 mM·kg–1 during the ischemia. Hyperglycemic animals displayed a more moderate rate of fall of PCr and ATP, with ATP values exceeding 50% of control after 2 min 30 s. Glycogen stores were largely maintained, but degradation of glucose somewhat enhanced the lactic acidosis. The results demonstrate that hyperglycemic rats maintained ATP at levels sufficient to prevent cell depolarization and calcium influx during the ischemic period. However, the metabolic perturbation observed must have been responsible for the delayed neuronal damage. We speculate that lowered ATP, increased inorganic P, and oxidative stress triggered a delayed mitochondrial permeability transition (MPT), which led to delayed neuronal necrosis. This assumption was supported by a second series of experiments in which CA1 damage in hyperglycemic rats was prevented by cyclosporin A, a virtually specific inhibitor of the MPT.
      datePublished:
      dateModified:
      pageStart:44
      pageEnd:50
      sameAs:https://doi.org/10.1007/PL00005622
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         Key words Forebrain ischemia
         Hyperglycemia
         Hippocampus
         Bioenergetic state
         Cyclosporin A
         Rat
         Neurosciences
         Neurology
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                     name:Laboratory for Experimental Brain Research, Experimental Research Center, Lund University, Lund, Sweden; Tel.: +46–46 173552, Fax: +46–46 151480, , SE
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