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First published online August 6, 2004
Journal of Experimental Biology 207, 3141-3147 (2004)
Published by The Company of Biologists 2004
doi: 10.1242/jeb.01056

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Negotiating brain anoxia survival in the turtle

Peter L. Lutz^* and Sarah L. Milton

Department of Biological Sciences, Florida Atlantic University, Boca Raton, FL 33431, USA

View larger version (10K): [in a new window]   Fig. 1. Progressive decrease in the rate of increase in extracellular K+ following ouabain superfusion in the anoxic turtle striatum (from Pek and Lutz, 1997).

View larger version (28K): [in a new window]   Fig. 2. A diagrammatic overview of some of the factors involved in negotiating anoxia survival in the turtle brain. Constitutive factors that predispose for anoxia tolerance include enhanced levels of glycogen stores, elevated heat shock protein, increased densities of protective receptors and elevated antioxidant capacities. Three distinct phases are involved in surviving and recovering from anoxia. (1) A coordinated downregulation of ATP demand processes to 20% of normoxic levels. This phase, which takes 1–2 h, includes a reduction in ion channel and electrical activities, a reduction in glutamate and dopamine release, a reduction in protein synthesis and a substantial increase in Hsp72 and Hsc73 levels. (2) Long-term survival (days) at basal levels of ATP expenditure. Neuronal network integrity is preserved through the continued operation of core activities. These include periodic electrical activity, an increased release of GABA and a reduced but continued release of glutamate and dopamine. There is a further increase in Hsc73, indicating a `housekeeping' role for this protein during this period. (3) When oxygen becomes available there is a rapid upregulation of neuronal processes to restore full function, together with the activation of protection mechanisms against reperfusion-generated reactive oxygen species (ROS).