Depolarizing effects of anoxia on pyramidal cells of rat neocortex.
The response of rat neocortical pyramidal neurons (layers II III) in vitro to brief periods of anoxia is a reversible depolarization of 3.8 +/- 1.01 mV (mean +/- S.E.M.; n = 114), which is accompanied by a moderate decrease in input resistance and significant depression of evoked synaptic activity. This effect is mimicked by ouabain, and is partially attenuated by the excitatory amino acid (EAA) antagonist, kynurenic acid. The estimated reversal potential (Vrev) for the anoxic depolarization (AD) is between -35 and -40 mV; in the presence of TTX a Vrev of -65 mV is obtained. Although a partial failure of Na(+)-K(+) pump activity and release of EAAs may contribute the generation of the AD, other processes are likely to be involved.
Rosen
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Department of Pharmacology, University of Ottawa, Canada.
Morris
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D000818:Animals; D015687:Cell Hypoxia / Q000187:drug effects / Q000502:physiology*; D002540:Cerebral Cortex / Q000502:physiology*; D005071:Evoked Potentials / Q000502:physiology; D006624:Hippocampus / Q000166:cytology / Q000502:physiology; D066298:In Vitro Techniques; D007736:Kynurenic Acid / Q000494:pharmacology; D010042:Ouabain / Q000494:pharmacology; D011712:Pyramidal Tracts / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D013779:Tetrodotoxin / Q000494:pharmacology
D013779:Tetrodotoxin; D010042:Ouabain; D000254:Sodium-Potassium-Exchanging ATPase; D007736:Kynurenic Acid