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

The release of excitatory amino acids such as glutamate contributes gr eatly to anoxic and/or ischemic brain damage in mammals. However, for anoxia-intolerant ectothermic vertebrates, there has been no informati on 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, us ing microdialysis and K+-selective microelectrodes. Systemic blood pre ssure was also monitored. In separate experiments, endogenous neurotra nsmitter release was provoked by perfusing the microdialysis probe wit h a high-K+ Ringer solution, thereby establishing which amino acids ar e released by depolarization. Anoxia exposure resulted in the release of several amino acids, including glutamate, aspartate, gamma-aminobut yric acid (GABA), glycine, and taurine. GABA release appeared to be de layed compared with that of glutamate, for example. The loss of ion ho meostasis (starting after 23 min) preceded the release of amino acids (starting after greater than or equal to 45 min). The amino acid relea se had no apparent effect on the rate of increase in extracellular K+. Thus, if these events are interrelated, the loss of ion homeostasis i s likely to trigger the amino acid release but not vice versa.