Prolonged anoxic depolarization exacerbates NADH hyperoxidation and promotes poor electrical recovery after anoxia in hippocampal slices

Prolonged anoxic depolarization exacerbates NADH hyperoxidation and promotes poor electrical... Mitochondrial dysfunction appears to occur during brain ischemia and following reperfusion. A characteristic event during reoxygenation after anoxia in hippocampal slices is hyperoxidation of the electron carriers of the mitochondrial respiratory chain. Earlier studies suggested that calcium influx due to loss of ion homeostasis during anoxia was linked to neuronal damage. Since a link between cytosolic calcium overload and post-anoxic hyperoxidation (PAMHo) has been suggested in previous studies, present studies sought to test the hypothesis that the length of anoxic depolarization can influence hyperoxidation and electrical activity recovery following anoxia in hippocampal slices. Rat hippocampal slices were made anoxic and then allowed to recover for 60 min. The time of anoxia was defined by the time of anoxic depolarization (AD), and slices were divided in five groups: 0.5, 1, 2, 5 and 10 min of AD. Reduction/oxidation shifts of NADH were measured by rapid scanning spectrofluorometry. Synaptic activity was indicated by population spike amplitudes in the CA1 pyramidal cell subfield of the hippocampus in response to stimulation of the Schaffer collaterals. We report here that mitochondrial hyperoxidation and synaptic activity in hippocampal slices are highly sensitive to the time in which slices remain depolarized (AD). http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Brain Research Elsevier

Prolonged anoxic depolarization exacerbates NADH hyperoxidation and promotes poor electrical recovery after anoxia in hippocampal slices

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Publisher
Elsevier
Copyright
Copyright © 1998 Elsevier Science B.V.
ISSN
0006-8993
DOI
10.1016/S0006-8993(97)01438-8
Publisher site
See Article on Publisher Site

Abstract

Mitochondrial dysfunction appears to occur during brain ischemia and following reperfusion. A characteristic event during reoxygenation after anoxia in hippocampal slices is hyperoxidation of the electron carriers of the mitochondrial respiratory chain. Earlier studies suggested that calcium influx due to loss of ion homeostasis during anoxia was linked to neuronal damage. Since a link between cytosolic calcium overload and post-anoxic hyperoxidation (PAMHo) has been suggested in previous studies, present studies sought to test the hypothesis that the length of anoxic depolarization can influence hyperoxidation and electrical activity recovery following anoxia in hippocampal slices. Rat hippocampal slices were made anoxic and then allowed to recover for 60 min. The time of anoxia was defined by the time of anoxic depolarization (AD), and slices were divided in five groups: 0.5, 1, 2, 5 and 10 min of AD. Reduction/oxidation shifts of NADH were measured by rapid scanning spectrofluorometry. Synaptic activity was indicated by population spike amplitudes in the CA1 pyramidal cell subfield of the hippocampus in response to stimulation of the Schaffer collaterals. We report here that mitochondrial hyperoxidation and synaptic activity in hippocampal slices are highly sensitive to the time in which slices remain depolarized (AD).

Journal

Brain ResearchElsevier

Published: Mar 9, 1998

References

  • Oxygen radicals in focal cerebral ischemia
    Chan, P.H.
  • Kinetics of microcirculatory, NAD/NADH, and electrocorticographic changes in cat brain cortex during ischemia and recirculation
    Dora, E.; Tanaka, K.; Greenberg, J.H.; Gonatas, N.H.; Reivich, M.
  • Hydroperoxide-induced oxidative stress impairs heart muscle cell carbohydrate metabolism
    Janero, D.R.; Hreniuk, D.; Sharif, H.M.
  • Intracellular redox changes in functioning cerebral cortex: I. Metabolic effects of epileptiform activity
    Jobsis, F.F.; O'Connor, M.; Vitale, A.; Vreman, H.
  • Metabolic, ionic, and electrical responses of gerbil brain to ischemia
    Mayevsky, A.; Friedli, C.M.; Reivich, M.
  • Extracellular potassium, volume fraction and tortuosity in rat hippocampal CA1, CA3 and cortical slices during ischemia
    Pérez-Pinzón, M.A.; Tao, L.; Nicholson, C.

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