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https://hdl.handle.net/2440/48807
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Type: | Journal article |
Title: | The metabolism of 14C-glucose by neurons and astrocytes in brain subregions following focal cerebral ischemia in rats |
Author: | Thoren, A. Helps, S. Nilsson, M. Sims, N. |
Citation: | Journal of Neurochemistry, 2006; 97(4):968-978 |
Publisher: | Blackwell Publishing Ltd |
Issue Date: | 2006 |
ISSN: | 0022-3042 1471-4159 |
Abstract: | To provide insights into the effects of temporary focal ischemia on the function of neurons and astrocytes in vivo, we measured the incorporation of radiolabel from [U-14C]glucose into both glutamate and glutamine in brain subregions at 1 h of reperfusion following occlusion of the middle cerebral artery for 2 or 3 h. Under the experimental conditions used, 14C-glutamate is mainly produced in neurons whereas 14C-glutamine is generated in astrocytes from 14C-glutamate of both neuronal and astrocytic origin. Radiolabel incorporation into both amino acids was greatly decreased. The change in 14C-glutamate accumulation provides strong evidence for substantial reductions in neuronal glucose metabolism. The resulting decrease in delivery of 14C-glutamate from the neurons to astrocytes was probably also the major contributor to the change in 14C-glutamine content. These alterations probably result in part from a marked depression of glycolytic activity in the neurons, as suggested by previous studies assessing deoxyglucose utilization. Alterations in 14C-glucose metabolism were not restricted to tissue that would subsequently become infarcted. Thus, these changes did not inevitably lead to death of the affected cells. The ATP : ADP ratio and phosphocreatine content were essentially preserved during recirculation following 2 h of ischemia and showed at most only moderate losses in some subregions following 3 h of ischemia. This retention of energy reserves despite the decreases in 14C-glucose metabolism in neurons suggests that energy needs were substantially reduced in the post-ischemic brain. Marked increases in tissue lactate accumulation during recirculation, particularly following 3 h of ischemia, provided evidence that impaired pyruvate oxidation probably also contributed to the altered 14C-glucose metabolism. These findings indicate the presence of complex changes in energy metabolism that are likely to greatly influence the responses of neurons and astrocytes to temporary focal ischemia. |
DOI: | 10.1111/j.1471-4159.2006.03778.x |
Published version: | http://dx.doi.org/10.1111/j.1471-4159.2006.03778.x |
Appears in Collections: | Aurora harvest Pathology publications |
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