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AJP - Regulatory, Integrative and Comparative Physiology, Vol 257, Issue 4 854-R860, Copyright © 1989 by American Physiological Society
ARTICLES |
C. P. Chih, Z. C. Feng, M. Rosenthal, P. L. Lutz and T. J. Sick
Department of Neurology, University of Miami, School of Medicine 33101.
Unlike the mammalian brain, the turtle brain maintains ion homeostasis and avoids anoxic depolarization during prolonged anoxia. The mechanisms by which turtle brains avoid and recover from anoxic depolarization were investigated by relating changes in cellular ATP levels to extracellular K+ (K+o) and evoked potential activities after 6 h of anoxia and during anoxic depolarization induced by superfusion of the brain surface with iodoacetate during anoxia. ATP levels were maintained during 6 h of anoxia despite marked decreases in energy production, but ATP was lowered during inhibition of both oxidative phosphorylation and glycolysis. K+o activity was unchanged during 6 h of anoxia but increased when ATP levels decreased. Ion homeostasis in the turtle brain appears to be linked to ATP levels but is unaffected by rate of energy production. In contrast, amplitudes of evoked potentials decreased when ATP levels were maintained, but rate of energy production declined. ATP and K+o levels recovered after anoxic depolarization, but evoked potential activity was not restored. These data suggest that the basic strategy for turtle brain to survive anoxia is to avoid anoxic depolarization by maintaining ATP levels.
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