ROLES OF ENERGY STATUS, K-ATP CHANNELS AND CHANNEL ARREST IN FISH BRAIN K+ GRADIENT DISSIPATION DURING ANOXIA

The crucian carp (Carassius carassius L.) is one of the most anoxia-to lerant vertebrates known, being able to maintain ion homeostasis in it s brain for many hours of anoxia. This study aims to clarify the impor tance of glycolysis during anoxia and also to investigate whether the extreme tolerance to anoxia could be due to downregulation of K+ perme ability ('channel arrest') and/or activation of ATP-sensitive K+ (K-AT P) channels. The latter was also tested in rainbow trout (Oncorhynchus mykiss). The results suggest that, during anoxia, the crucian carp br ain is completely dependent on glycolysis, since blocking glycolysis w ith iodoacetic acid (IAA) rapidly caused an increase in [K+](0) that c oincided with a drastic drop in ATP level and energy charge. Testing t he channel arrest hypothesis by measuring the K+ efflux rate after Na/K+-ATPase had been blocked by ouabain revealed no change in K+ permea bility in crucian carp brain in response to anoxia. Furthermore, super fusing the brain of anoxic crucian carp with the K-ATP channel blocker glibenclamide did not alter the efflux rate of K+ after glycolysis ha d been inhibited with IAA. Glibenclamide had no effect on K+ efflux ra te in rainbow trout brain during anoxia.