Nitric oxide is involved in anoxic preconditioning neuroprotection in rat hippocampal slices

Sublethal anoxia/ischemia protects against subsequent damaging insults in intact brain or hippocampal slices. To help further understand mechanisms underlying anoxic/ischemic preconditioning, we tested three hypotheses which were that: (a) anoxic preconditioning (APC) improves electrical recovery in rat hippocampal slices; (b) anoxic preconditioning requires nitric oxide (NO); and (c) anoxic preconditioning blocks mitochondrial dysfunction that occurs following re-oxygenation after anoxia. Control hippocampal slices underwent a single `test' anoxic insult. Experimental slices were preconditioned by 3 short anoxic insults prior to the `test' insult. Evoked potentials (EPs), and NADH redox status were recorded prior to, during and after preconditioning and/or `test' anoxic insults. To examine the role of NO, studies sought to determine whether APC could be produced by the NO donor, DEA/NO, and whether APC could be inhibited by NO synthase (NOS) inhibitor (7-nitroindazole). EP amplitudes recovered significantly better after reoxygenation in preconditioned slices and after NO-emulated preconditioning (90.0±17.7% and 90.0±21.3%, respectively, n=9, ** p