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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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Review Article

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

^* Author for correspondence (e-mail: lutz{at}fau.edu)

Accepted 26 April 2004

The turtle brain's extraordinary ability to tolerate anoxia is based on constitutive and expressed factors. Constitutive factors that predispose for anoxia tolerance include enhanced levels of glycogen stores, increased densities of protective receptors, elevated antioxidant capacities and elevated heat shock protein. However, to survive an anoxic insult, three distinct phases must be negotiated successfully. (1) A coordinated downregulation of ATP demand processes to basal levels. This phase, which takes 1–2 h, includes a reduction in voltage-gated K⁺ (Kv) channel transcription and a substantial increase in Hsp72 and Hsc73 levels. During this period, adenosine and K_ATP channels mediate several key events including channel arrest initiation and a reduction in the release of excitatory amino acids (EAAs). (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 continued release of glutamate and dopamine. Adenosine and GABA modulate the glutamate release. There is a further increase in Hsc73, indicating a `housekeeping' role for this protein during this period. (3) A rapid upregulation of neuronal processes when oxygen becomes available to restore full function, together with the activation of protection mechanisms against reperfusion-generated reactive oxygen species.

Key words: anoxia tolerance, ATP expenditure, GABA, heat shock protein, turtle, Trachemys scripta

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THE HYPOXIC BRAIN

Kathryn Phillips
JEB 2004 207: i. [Full Text]  

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