Anoxia-tolerant vertebrates decrease their metabolic rate by 70% or more during anoxia, while the major inhibitory neurotransmitter in the vertebrate brain, GABA, increases in concentration. To test the possibility that GABA could be a mediator of anoxic metabolic depression, crucian carp (Carassius carassius L.) were given an inhibitor of GABA synthesis, isoniazid, and the rate of anoxic ethanol production (ethanol being the main end product of energy metabolism in anoxic crucian carp) as well as the rates of normoxic and hypoxic oxygen consumption were measured. Isoniazid (500mgkg−1), which significantly inhibited the anoxia-induced rise in brain GABA concentration, caused a nearly threefold increase in anaerobic ethanol production without affecting normoxic oxygen consumption. The GABA synthesis inhibitor 3-mercaptopropionic acid (3-MP, 200mgkg−1) and the GABA receptor antagonist securinine (20mgkg−1) caused similar rises in anoxic ethanol production. Nevertheless, crucian carp given 250–500mgkg−1 isoniazid, 200mgkg−1 3-MP or 20mgkg−1 securinine all recovered after anoxia, suggesting that a complete depression of the rate of metabolism may not be essential for survival during short-term anoxia. These results indicate that GABA is a mediator of anoxic metabolic depression in crucian carp.

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