NeurophysiologyContribution of GABAA-mediated conductances to anoxia-induced depolarizationD'Antuono, Margherita1,2; Kawasaki, Hiroto1; Tancredi, Virginia2; Avoli, Massimo1,3Author Information 1Montréal Neurological Institute and Departments of Neurology and Neurosurgery and Physiology, McGill University, 3801 University St, Montréal, Québec, H3A 2B4, Canada 2Dipartimento di Neuroscienze, Universitá degli Studi di Roma ‘Tor Vergata’, 00173, Roma, Italy 3Corresponding Author: Massimo Avoli ACKNOWLEDGEMENTS: This work was supported by the Medical Research Council of Canada (MT-8109) and the Quebec Heart and Stroke Foundation. Received 26 August 1998; accepted 22 October 1998 NeuroReport: December 21st, 1998 - Volume 9 - Issue 18 - p 4189-4192 Buy Abstract CA1 pyramids were studied intracellularly in rat hippocampal slices to establish the contribution of excitatory amino acid (EAA) and GABAA receptors to the depolarizations induced by brief ± 10 min) anoxic episodes. An increase of the amplitude of the depolarizations evoked by successive anoxic episodes occurred with KCl (n = 4 cells), not with K-acetate-filled (n = 3) recording electrodes. Moreover, with K-acetate-filled electrodes the anoxic depolarization amplitude was reduced, but not abolished by EAA receptor antagonists (n = 14). The residual anoxic depolarizations were blocked by a GABAA receptor antagonist (n = 5) and decreased by the carbonic anhydrase inhibitor acetazolamide (n = 4). We conclude that the anoxic depolarizations generated by CA1 pyramids are caused by the activation of EAA along with GABAA receptors leading to an increased membrane conductance to both Cl− and HCO3−. © 1998 Lippincott Williams & Wilkins, Inc.