Contribution of GABA(A)-mediated conductances to anoxia-induced depolarization

CA1 pyramids were studied intracellularly in rat hippocampal slices to esta blish the contribution of excitatory amino acid (EAA) and GABA, receptors t o the depolarizations induced by brief (< 10 min) anoxic episodes. An incre ase of the amplitude of the depolarizations evoked by successive anoxic epi sodes occurred with KCI (n = 4 cells), not with K-acetate-filled (n = 3) re cording electrodes. Moreover, with K-acetate-filled electrodes the anoxic d epolarization amplitude was reduced, but not abolished by EAA receptor anta gonists (n = 14). The residual anoxic depolarizations were blocked by a GAB A, receptor antagonist (n = 5) and decreased by the carbonic anhydrase inhi bitor acetazolamide (n = 4). We conclude that the anoxic depolarizations ge nerated by CA1 pyramids are caused by the activation of EAA along with GABA , receptors leading to an increased membrane conductance to both Cl- and HC O3-. (C) 1998 Lippincott Williams & Wilkins.