Anoxic preconditioning in hippocampal slices: role of adenosine

Prior studies have shown that sublethal anoxic/ischemic insults may “precondition” and thereby protect tissues such as heart and brain from subsequent insults. In hippocampal slices, we examined two hypotheses: (i) that anoxic preconditioning improves the ability of slices to recover synaptic activi...

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Bibliographic Details
Published in:Neuroscience Vol. 75; no. 3; pp. 687 - 694
Main Authors: Péerez-pinzón, M.A., Mumford, P.L., Rosenthal, M., Sick, T.J.
Format: Journal Article
Language:English
Published: Oxford Elsevier Ltd 01-12-1996
Elsevier
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Summary:Prior studies have shown that sublethal anoxic/ischemic insults may “precondition” and thereby protect tissues such as heart and brain from subsequent insults. In hippocampal slices, we examined two hypotheses: (i) that anoxic preconditioning improves the ability of slices to recover synaptic activity following a second anoxic insult and (ii) that anoxic preconditioning involves adenosine receptors. Hippocampal slices were preconditioned by short periods of anoxia prolonged only until the onset of anoxic depolarization. The slices were then reoxygenated for 30 min, after which a second (“test”) anoxic insult was induced. Amplitudes of evoked potentials recovered significantly better after “test” anoxic insults in preconditioned slices. In control slices, transient superfusion with adenosine or an adenosine A1 receptor agonist (2-chloroadenosine) 30 min prior to “test” anoxia markedly improved evoked potential recovery. Administration of 8-cyclopentyl-1 3-dipropylxanthine, an Al receptor antagonist, blocked the protection afforded by preconditioning. These data support the hypothesis that adenosine, probably by its activation of Al receptors, is involved in the neuroprotection afforded by anoxic preconditioning in hippocampal slices. Preconditioning insults may have a significant clinical impact, since certain surgical procedures may require, or produce, multiple periods of brain ischemia.
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ISSN:0306-4522
1873-7544
DOI:10.1016/0306-4522(96)00311-9