Abstract

ABSTRACT In the brain of most vertebrates, anoxia or ischaemia rapidly causes a fall in ATP levels and in the activity of the Na+/K+ pump, resulting in general depolarization followed by a cascade of catastrophic events (Hansen, 1985; Hochachka, 1986). By contrast, the brain of freshwater turtles survives many hours of complete anoxia at 25°C. Hence, the turtle brain has become the archetype of an anoxia-tolerant brain, and considerable efforts have been devoted to finding the mechanisms underlying its exceptional ability to survive without oxygen. The turtle brain’s main strategy for anoxic survival seems to be to decrease energy utilization, so that ATP consumption can be met by glycolytic ATP production alone (Sick et al. 1982; Lutz et al. 1985; Chih et al. 1989). However, the mechanisms mediating the lowered energy consumption have remained obscure.

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