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Am J Physiol Regul Integr Comp Physiol (December 21, 2001). doi:10.1152/ajpregu.00484.2001
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Articles in PresS, published online ahead of print December 21, 2001
Am J Physiol Regu Physiol, 10.1152/ajpregu.00484.2001
Submitted on August 9, 2001
Accepted on December 11, 2001

Mechanisms for maintaining extracellular glutamate levels in the anoxic turtle striatum

Sarah L Milton1*, John W Thompson1, and Peter L Lutz1

1 Dept. of Biological Sciences, Florida Atlantic University, Boca Raton, FL, USA

* To whom correspondence should be addressed. E-mail: smilton{at}fau.edu.

The turtle Trachemys scripta is one of a limited group of vertebrates which can withstand hours to days without oxygen. One facet of anoxic survival is the turtle's ability to maintain basal extracellular glutamate levels, whereas in most vertebrates anoxia triggers massive excitotoxic glutamate release. We investigated glutamate release and reuptake in the anoxic turtle and the effects of adenosine and ATP-sensitive potassium channels (KATP) on glutamate homeostasis. Striatal extracellular glutamate was measured in anesthetized T. scripta by microdialysis in normoxia and over 2 hr anoxia. Glutamate release decreased by 44% in the early anoxic turtle; this anoxia-induced decrease in glutamate release was prevented when KATP channels and adenosine receptors were blocked simultaneously, but not when either mechanism was blocked individually. We hypothesize that the continued release and reuptake of glutamate during anoxia helps maintain neuronal tone and aids in the recovery of a functional neuronal network after long periods of anoxia, while activation of adenosine and/or KATP conserves energy by reducing glutamate release and lowering transport costs.




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