Metabolic mechanisms of anoxia tolerance in the turtle brain.

Abstract

Turtle brain survives anoxia by maintaining ATP levels necessary to avoid the loss of ion homeostasis and the uncontrolled release of excitotoxic neurotransmitters [1–6]. A central question toward defining anoxic tolerance in turtle brain is how do ATP production and ATP use remain matched despite complete inhibition of oxidative metabolism. Indirect evidence of both a Pasteur effect and a hypometabolic state have been proposed previously. For example, calculations based on creatine phosphate depletion and lactate accumulation during anoxia suggested that ATP production was markedly reduced (by approx 88%) [1, 2]. Also, enzymatic studies of turtle brain suggested the presence of an initial Pasteur effect followed by a decrease in the glycolytic rate[7]. Depression of electrical activity in the turtle brain further strengthened the proposal of the presence of a hypometabolic state [5, 8–10].