title: Anoxic depolarization of hippocampal astrocytes: possible modulation by P2X7 receptors.
abstract: Current responses from CA1 neurons and stratum oriens astrocytes were recorded from hippocampal brain slices by means of the whole-cell patch-clamp technique. Anoxic depolarization (AD) was induced by an oxygen/glucose-deprived (OGD) medium also containing sodium iodoacetate and antimycin, in order to block glycolysis and oxidative phosphorylation, respectively. Anoxic depolarization has been reported to be due to the sudden increase of the extracellular K(+) concentration and the accompanying explosive rise in glutamate concentration. We asked ourselves whether the release of ATP activating P2X7 receptors is also involved in the AD. Although, the AD was evoked in absolute synchrony in neurons and astrocytes, and the NMDA receptor antagonistic AP-5 depressed these responses, neither the non-selective P2 receptor antagonist PPADS, nor the highly selective P2X7 receptor antagonist A438079 interfered with the AD or its delay time in neurons/astrocytes after inducing chemical hypoxia. However, A438079, but not PPADS increased in astrocytes the slow inward current observed in a hypoxic medium. It is concluded that ATP co-released with glutamate by hypoxic stimulation has only a minor function in the present brain slice system.
authors.affiliation: Rudolf-Boehm-Institute of Pharmacology and Toxicology, University of Leipzig, D-04107 Leipzig, Germany.
authors.forename: Anna
authors.initials: A
authors.lastname: Leichsenring
authors.forename: Thomas
authors.initials: T
authors.lastname: Riedel
authors.forename: Ying
authors.initials: Y
authors.lastname: Qin
authors.forename: Patrizia
authors.initials: P
authors.lastname: Rubini
authors.forename: Peter
authors.initials: P
authors.lastname: Illes
mesh_terms: D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001253:Astrocytes / Q000187:drug effects / Q000502:physiology*; D056547:CA1 Region, Hippocampal / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D015687:Cell Hypoxia / Q000502:physiology*; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D005971:Glutamates / Q000378:metabolism; D006624:Hippocampus / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D066298:In Vitro Techniques; D007473:Ion Channels / Q000187:drug effects; D009474:Neurons / Q000187:drug effects; D018408:Patch-Clamp Techniques; D058920:Purinergic P2X Receptor Antagonists / Q000494:pharmacology; D058912:Purinergic P2Y Receptor Agonists / Q000494:pharmacology; D011725:Pyridines / Q000494:pharmacology; D011732:Pyridoxal Phosphate / Q000031:analogs & derivatives / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors; D058486:Receptors, Purinergic P2X7 / Q000187:drug effects*; D013777:Tetrazoles / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology
chemical_list: C523668:3-(5-(2,3-dichlorophenyl)-1H-tetrazol-1-yl)methylpyridine; D018691:Excitatory Amino Acid Antagonists; D005971:Glutamates; D007473:Ion Channels; D058920:Purinergic P2X Receptor Antagonists; D058912:Purinergic P2Y Receptor Agonists; D011725:Pyridines; D016194:Receptors, N-Methyl-D-Aspartate; D058486:Receptors, Purinergic P2X7; D013777:Tetrazoles; C077792:pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid; D013779:Tetrodotoxin; D011732:Pyridoxal Phosphate; D015763:2-Amino-5-phosphonovalerate; D000255:Adenosine Triphosphate