Direct mapping of super(19)F in super(19)FDG-6P in brain tissue at subcellular resolution using soft X-ray fluorescence

Low energy x-ray fluorescence (LEXRF) detection was optimized for imaging cerebral glucose metabolism by mapping the fluorine LEXRF signal of super(19)F in super(19)FDG, trapped as intracellular super(19)F-deoxyglucose-6-phosphate ( super(19)FDG-6P) at l mu m spatial resolution from 3 mu m thick bra...

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Bibliographic Details
Published in:Journal of physics. Conference series 2013-01, Vol.463, p.1-7
Main Authors: Poitry-Yamate, C, Gianoncelli, A, Kourousias, G, Kaulich, B, Lepore, M, Gruetter, R, Kiskinova, M
Format: Article
Language:English
Subjects:
Brain
Glucose
Imaging
Mapping
Metabolism
Neurons
Positron emission
Tomography
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Summary:Low energy x-ray fluorescence (LEXRF) detection was optimized for imaging cerebral glucose metabolism by mapping the fluorine LEXRF signal of super(19)F in super(19)FDG, trapped as intracellular super(19)F-deoxyglucose-6-phosphate ( super(19)FDG-6P) at l mu m spatial resolution from 3 mu m thick brain slices. super(19)FDG metabolism was evaluated in brain structures closely resembling the general cerebral cytoarchitecture following formalin fixation of brain slices and their inclusion in an epon matrix. 2-dimensional distribution maps of super(19)FDG-6P were placed in a cytoarchitectural and morphological context by simultaneous LEXRF mapping of N and O, and scanning transmission x-ray (STXM) imaging. A disproportionately high uptake and metabolism of glucose was found in neuropil relative to intracellular domains of the cell body of hypothalamic neurons, showing directly that neurons, like glial cells, also metabolize glucose. As super(19)F-deoxyglucose-6P is structurally identical to super(18)F-deoxyglucose-6P, LEXRF of subcellular super(19)F provides a link to in vivo super(18)FDG PET, forming a novel basis for understanding the physiological mechanisms underlying the super(18)FDG PET image, and the contribution of neurons and glia to the PET signal.
ISSN:1742-6588
1742-6596
DOI:10.1088/1742-6596/463/1/012003