Nilsson G E, Lutz P L
Rosenstiel School of Marine and Atmospheric Science, University of Miami, Florida 33149-1098.
Am J Physiol. 1991 Jul;261(1 Pt 2):R32-7. doi: 10.1152/ajpregu.1991.261.1.R32.
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.
在哺乳动物中，兴奋性神经递质谷氨酸在缺氧/缺血几分钟内大量释放，被认为是缺氧性脑损伤的主要介质。与哺乳动物的大脑不同，龟脑对缺氧具有极强的耐受性。通过对龟脑纹状体进行脑内微透析，我们发现在缺氧期间抑制性神经递质γ-氨基丁酸的细胞外水平大幅增加，240分钟后达到常氧水平的90倍，而谷氨酸并未大量释放。此外，抑制性神经递质/神经调质甘氨酸和牛磺酸在缺氧期间细胞外水平也有所增加。抑制性氨基酸细胞外水平的增加可能是迄今为止难以捉摸的机制之一，它构成了缺氧龟脑活动和能量消耗降低的基础。
