Journal article
Contribution of GABA(A)-mediated conductances to anoxia-induced depolarization
Neuroreport, Vol.9(18), pp.4189-4192
12/21/1998
DOI: 10.1097/00001756-199812210-00034
PMID: 9926871
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-.
Details
- Title: Subtitle
- Contribution of GABA(A)-mediated conductances to anoxia-induced depolarization
- Creators
- M D'Antuono - Montréal Neurological Institute and Department of Neurology and Neurosurgery, McGill University, Québec, CanadaH KawasakiV TancrediM Avoli
- Resource Type
- Journal article
- Publication Details
- Neuroreport, Vol.9(18), pp.4189-4192
- DOI
- 10.1097/00001756-199812210-00034
- PMID
- 9926871
- ISSN
- 0959-4965
- eISSN
- 1473-558X
- Language
- English
- Date published
- 12/21/1998
- Academic Unit
- Neurosurgery
- Record Identifier
- 9984083297302771
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