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Am J Physiol Regul Integr Comp Physiol 260: R747-R755, 1991;
0363-6119/91 $5.00
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AJP - Regulatory, Integrative and Comparative Physiology, Vol 260, Issue 4 747-R755, Copyright © 1991 by American Physiological Society

ARTICLES

Effects of anoxia and metabolic arrest on turtle and rat cortical neurons

C. J. Doll, P. W. Hochachka and P. B. Reiner
Department of Zoology, University of British Columbia, Vancouver, Canada.

The responses of turtle and rat cortical pyramidal neurons to various pharmacological treatments were measured using intracellular recordings. Turtle neurons survived both anoxia and pharmacological anoxia for 180 min with no noticeable effect. Rat pyramidal neurons responded with a loss in membrane resistance, followed by a transient hyperpolarization, and a subsequent depolarization to a zero membrane potential (41.3 +/- 6.5 min, anoxia; 25.8 +/- 12.6 min, pharmacological anoxia). Metabolic arrest caused a rapid loss in membrane resistance, transient hyperpolarization, and a rapid depolarization in both turtle (4.6 +/- 1.1 min) and rat (3.1 +/- 0.5 min) neurons. Iodoacetate alone had a similar effect on the rat as metabolic arrest (6.5 +/- 0.8 min), but the turtle exhibited more prolonged survival (53.5 +/- 4.6 min). Ouabain caused a rapid depolarization in the rat cortical neuron (8.6 +/- 1.1 min), but no initial loss in membrane resistance or a hyperpolarization. These results demonstrate that the turtle neuron, which survives anoxia, is no better at surviving total metabolic inhibition than the rat neuron. In addition, anoxia takes 13 times longer to depolarize a rat cortical neuron than metabolic arrest, and neither of these treatments is totally mimicked by ouabain alone.


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