Krnjevic_1991_Neurochem.Res_16_279

In rat hippocampal slices GABAergic IPSPs are very rapidly suppressed by anoxia (in less than 2 min). Both early (GABAA) and late (GABAB) components are affected. After reoxygenation, the IPSPs recover, but only slowly and not always completely. Iontophoretic applications of GABA or baclofen indicated no major depression of responses during anoxia. It is therefore unlikely that the anoxic suppression of IPSPs is caused by desensitizations of GABA receptors. A more probable explanation is a failure of GABAergic neurons to release GABA from inhibitory nerve terminals.