Short Communication Adenosine Release in the Anoxic Turtle Brain: a Possible Mechanism for Anoxic Survival

In the brain of most vertebrates, anoxia or ischaemia rapidly causes a fall in ATP levels and in the activity of the Na + /K + pump, resulting in general depolarization followed by a cascade of catastrophic events (Hansen, 1985; Hochachka, 1986). By contrast, the brain of freshwater turtles survives many hours of complete anoxia at 25°C. Hence, the turtle brain has become the archetype of an anoxia-tolerant brain, and considerable efforts have been devoted to finding the mechanisms underlying its exceptional ability to survive without oxygen. The turtle brain's main strategy for anoxic survival seems to be to decrease energy utilization, so that ATP consumption can be met by glycolytic ATP production alone (Sick et al. 1982; Lutz etal. 1985; Chih et al. 1989). However, the mechanisms mediating the lowered energy consumption have remained obscure. Neurotransmitters are ubiquitous regulators of brain activity. We recently found that, in response to anoxia, the turtle brain increases the levels of the inhibitory neurotransmitters/neuromodulators y-aminobutyric acid (GABA), glycine and taurine, while simultaneously reducing the level of the excitatory neurotransmitter glutamate (Nilsson etal. 1990). Moreover, by the use of microdialysis, we have also observed increases in the extracellular concentrations of GABA, glycine and taurine in the anoxic turtle brain (Nilsson and Lutz, 1991). However, the increase in the tissue levels of these inhibitory amino acids were relatively slow, and their release to the extracellular space was only apparent after about 100 min of anoxia. Thus, while inhibitory amino acids may be important mediators of the long-term suppression of energy use seen in anoxic turtles, they are not likely to be responsible for the initial early decrease in brain activity needed to meet a falling rate of ATP production. Consequently, we started to look for another inhibitory factor that would show a faster response to anoxia. One such factor could be adenosine, a product of the