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Article type: Research Article
Authors: Rüthrich, Heide-Linde | Krug, Manfred
Affiliations: Institute of Pharmacology and Toxicology, Medical Faculty, Otto-von-Guericke-University, Magdeburg, Germany
Note: [] Corresponding author: Dr. Heide-Linde Rüthrich, Institute of Pharmacology and Toxicology, Medical Faculty, Otto-von-Guericke-University, Leipziger Str. 44, D-39120 Magdeburg, Germany. Phone: +49 391 67 15878; Fax: +49 391 67 15869; E-mail: [email protected]
Abstract: Purpose: At present the mechanisms of ischemic or hypoxic tolerance are not fully understood at the cellular level. Methods: In order to further characterize the effects of conditioning hypoxia on the synaptic transmission in the hippocampal area CA1, rats were exposed to a moderate normobaric hypoxia for 8 h. Transverse hippocampal slices were prepared 1, 7 or 14 days after this conditioning hypoxia and evoked field potentials were recorded in the CA 1 region upon stimulation of the Schaffer collaterals before, during and up to 4 h after ischemia in vitro (hypoxia and reduced glucose). Results and Conclusions: The time to disappearance of the evoked potential during ischemia was significantly prolonged after seven, but not after one or 14 days in slices taken from conditioned animals. In addition the input/output (I/O) curves of evoked potentials were not altered 4 h after the ischemia. In contrast, the time to disappearance of the evoked potentials was shorter and the I/O curves were diminished in slices from control animals. Possible mechanisms of the protective effect are discussed.
Keywords: Hippocampal slices, hypoxia, ischemia, neuroprotection, field potentials, rat
Journal: Restorative Neurology and Neuroscience, vol. 15, no. 4, pp. 327-335, 1999
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