The crucian carp is one of the few vertebrates that has the ability to survive long periods of anoxia. A devastating event in the anoxic mammalian brain is a massive release of excitatory neurotransmitters, particularly glutamate. Using microdialysis to measure extracellular levels of several amino acid neurotransmitters and related compounds in the telencephalon of crucian carp in vivo, we show here that this species avoids a release of glutamate during anoxia, which is probably related to its ability to maintain energy charge. Instead, 6 h of anoxia produced a doubling of the extracellular level of GABA, the major inhibitory neurotransmitter in brain. The release of GABA may be a mechanism for lowering neuronal activity and energy use, thereby facilitating the maintenance of energy charge. Perfusing the microdialysis probe with a high-K+ Ringer showed that the telencephalon had the ability to release both glutamate and GABA. Moreover, if energy deficiency was produced during anoxia, by inhibiting glycolysis with iodoacetate (IAA), the resulting release of GABA was more rapid and profound than that of glutamate, possibly reflecting a second line of anoxia defence aimed at minimising the effect of a temporary energy failure.
Copyright 1999 Elsevier Science B.V.