Abstract
In mammals a massive release of the excitatory neurotransmitter glutamate, occurring within a few minutes of anoxia/ischemia, is thought to be a major mediator of anoxic brain damage. In contrast to the mammalian brain, the turtle brain is exceptionally anoxia tolerant. Using intracerebral microdialysis in turtle brain striatum, we have found a large increase in the extracellular level of the inhibitory neurotransmitter gamma-aminobutyric acid during anoxia, reaching 90 times the normoxic level after 240 min, whereas no substantial release of glutamate occurred. Moreover, the inhibitory neurotransmitters/neuromodulators glycine and taurine also displayed increased extracellular levels during anoxia. Increased extracellular levels of inhibitory amino acids may be one of the hitherto elusive mechanisms that underlie the decreased activity and energy consumption characterizing the anoxic turtle brain.
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Schedule a callMore From: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
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