CA1 pyramids were studied intracellularly in rat hippocampal slices to establish the contribution of excitatory amino acid (EAA) and GABAAreceptors 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 GABAAreceptor 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 GABAAreceptors leading to an increased membrane conductance to both Cl−and HCO3−.