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].
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Pérez-Pinzón, M.A., Lutz, P.L., Sick, T.J., Rosenthal, M. (1997). Metabolic Mechanisms of Anoxia Tolerance in the Turtle Brain. In: Nemoto, E.M., et al. Oxygen Transport to Tissue XVIII. Advances in Experimental Medicine and Biology, vol 411. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5865-1_9
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