Anoxic brain failure in an ectothermic vertebrate: release of amino acids and k+ in anoxic rainbow trout thalamus. Hylland, Patrick, G[diaeresis]oran E. Nilsson, and Dan Johansson. Vertebrate Physiology and Behaviour Unit, Department of Limnology, Uppsala University, Norbyv[umlaut]agen 20, S-752 36 Uppsala, SWEDEN
APStracts 2:0156R, 1995.
The release of excitatory amino acids such as glutamate contributes greatly to anoxic/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 C, using microdialysis and K+-selective microelectrodes. Also systemic blood pressure was monitored. In separate experiments, endogenous neurotransmitter release was provoked by perfusing the microdialysis probe with a high-K+ Ringer solution, thereby establishing what amino acids are released by depolarization. Anoxia exposure resulted in the release of several amino acids, including glutamate, aspartate, GABA, glycine and taurine. The GABA release appeared to be delayed compared to that of, for example, glutamate. The loss of ion-homeostasis (starting after 23 min) preceded the release of amino acids (starting after 45 min or more). 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. 

Received 15 November 1994; accepted in final form 2 June 1995.
APS Manuscript Number R657-4.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on  6 July 1995.