ANOXIC BRAIN FAILURE IN AN ECTOTHERMIC VERTEBRATE - RELEASE OF AMINO-ACIDS AND K+ IN RAINBOW-TROUT THALAMUS

The release of excitatory amino acids such as glutamate contributes greatly to anoxic and/or ischemic brain damage in mammals. However, for anoxia-intolerant ectothermic vertebrates, there has been no information on how anoxia affects extracellular amino acid levels, or how such changes relate temporally to major ion movements. We have investigated the effects of environmental anoxia on extracellular amino acid and K+ concentrations in rainbow trout thalamus in vivo at 15 degrees C, using microdialysis and K+-selective microelectrodes. Systemic blood pressure was also monitored. In separate experiments, endogenous neurotransmitter release was provoked by perfusing the microdialysis probe with a high-K+ Ringer solution, thereby establishing which amino acids are released by depolarization. Anoxia exposure resulted in the release of several amino acids, including glutamate, aspartate, gamma-aminobutyric acid (GABA), glycine, and taurine. GABA release appeared to be delayed compared with that of glutamate, for example. The loss of ion homeostasis (starting after 23 min) preceded the release of amino acids (starting after greater than or equal to 45 min). The amino acid release had no apparent effect on the rate of increase in extracellular K+. Thus, if these events are interrelated, the loss of ion homeostasis is likely to trigger the amino acid release but not vice versa.