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Journal of Experimental Biology, Vol 200, Issue 13 1913-1917, Copyright © 1997 by Company of Biologists
JOURNAL ARTICLES |
M Pek and PL Lutz
Department of Biological Sciences, Florida Atlantic University, Boca Raton 33431, USA.
The remarkable ability of the turtle brain to survive anoxia is based on its ability to match energy demand flexibly to energy production. Earlier studies indicate that reduced ion leakage is an important mechanism for energy conservation during anoxia. We tested the hypothesis that extracellular adenosine plays a role in the reduction of K+ flux (channel arrest) that occurs in the anoxic turtle brain. Changes in extracellular K+ concentration ([K+]o in the in situ brain of the turtle Trachemys scripta were monitored following inhibition of Na+/K(+)-ATPase with ouabain. The time to reach full depolarization ([K+]o plateau) was three times longer in the anoxic brain than in normoxic controls and the initial rate of K+ leakage was reduced by approximately 70%. Superfusing the brain before the during anoxia with the general adenosine receptor blocker theophylline, or the specific adenosine A1 receptor blocker 8-cyclopentyltheophylline, significantly shortened the time to full depolarization in the ouabain-challenged anoxic brain and increased the rate of K+ efflux. The results suggest that adenosine A1 receptors are involved in the expression of anoxia-induced ion channel arrest in the turtle brain.
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G Krumschnabel, C Biasi, and W Wieser Action of adenosine on energetics, protein synthesis and K(+) homeostasis in teleost hepatocytes J. Exp. Biol., January 9, 2000; 203(17): 2657 - 2665. [Abstract] [PDF]
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P. E. Bickler Reduction of NMDA receptor activity in cerebrocortex of turtles (Chrysemys picta) during 6 wk of anoxia Am J Physiol Regulatory Integrative Comp Physiol, July 1, 1998; 275(1): R86 - R91. [Abstract] [Full Text] [PDF]
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