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The crucian carp (Carassius carassius L.) is one of the most anoxia-tolerant vertebrates known, being able to maintain ion homeostasis in its brain for many hours of anoxia. This study aims to clarify the importance of glycolysis during anoxia and also to investigate whether the extreme tolerance to anoxia could be due to down-regulation of K+ permeability ('channel arrest') and/or activation of ATP-sensitive K+ (KATP) channels. The latter was also tested in rainbow trout (Oncorhynchus mykiss). The results suggest that, during anoxia, the crucian carp brain is completely dependent on glycolysis, since blocking glycolysis with iodoacetic acid (IAA) rapidly caused an increase in [K+]o that coincided with a drastic drop in ATP level and energy charge. Testing the channel arrest hypothesis by measuring the K+ efflux rate after Na+/K+-ATPase had been blocked by ouabain revealed no change in K+ permeability in crucian carp brain in response to anoxia. Furthermore, superfusing the brain of anoxic crucian carp with the KATP channel blocker glibenclamide did not alter the efflux rate of K+ after glycolysis had been inhibited with IAA. Glibenclamide had no effect on K+ efflux rate in rainbow trout brain during anoxia.

Roles of energy status, KATP channels and channel arrest in fish brain K+ gradient dissipation during anoxia