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

D'Antuono, M., Kawasaki, H., Tancredi, V., Avoli, M. (1998). Contribution of GABA(A)-mediated conductances to anoxia-induced depolarization. NEUROREPORT, 9(18), 4189-4192.

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

TANCREDI, VIRGINIA;
1998-12-21

Abstract

CA1 pyramids were studied intracellularly in rat hippocampal slices to establish the contribution of excitatory amino acid (EAA) and GABA(A) 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 GABA(A) 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 GABA(A) receptors leading to an increased membrane conductance to both Cl- and HCO3-.
21-dic-1998
Pubblicato
Rilevanza internazionale
Articolo
Esperti anonimi
Settore BIO/09 - FISIOLOGIA
English
Animals; Receptors, GABA-A; Pyramidal Cells; Electric Conductivity; Hippocampus; Bicuculline; Receptors, Amino Acid; Electrophysiology; Anoxia; Rats; Piperazines; Rats, Sprague-Dawley; Rats, Wistar; GABA-A Receptor Antagonists; Male; Excitatory Amino Acid Antagonists
D'Antuono, M., Kawasaki, H., Tancredi, V., Avoli, M. (1998). Contribution of GABA(A)-mediated conductances to anoxia-induced depolarization. NEUROREPORT, 9(18), 4189-4192.
D'Antuono, M; Kawasaki, H; Tancredi, V; Avoli, M
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/66816
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