Experimental ischemia induces a persistent depolarization blocked by decreased calcium and NMDA antagonists.
Early physiological events induced by hypoxia plus low D-glucose were investigated by intracellular recording in the rat hippocampal slice. A rapid intracellular depolarization corresponded to the extracellularly recorded anoxic depolarization. This intracellular depolarization consisted of two pharmacologically distinct components, an initial depolarization and a persistent depolarization. The persistent phase of depolarization was selectively blocked by lowering calcium and raising magnesium and by N-methyl-D-aspartate (NMDA) antagonists. This persistent depolarization can account for the long-term synaptic failure seen following experimental ischemia in vitro.
Rader
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Central Nervous System Diseases Research, G.D. Searle and Co., c/o Monsanto Co., St. Louis, MO 63198.
Lanthorn
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D000818:Animals; D002118:Calcium / Q000502:physiology*; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology*; D066298:In Vitro Techniques; D002546:Ischemic Attack, Transient / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D010879:Piperazines / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter / Q000187:drug effects / Q000502:physiology*
D010879:Piperazines; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter; C050592:3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid; D002118:Calcium