We utilized proton magnetic resonance spectroscopy to evaluate the metabolic profile of the hippocampus and anterior cingulate cortex of the developing rat brain from postnatal days 14-70. Measured metabolite concentrations were modeled using linear, exponential, or logarithmic functions and the time point at which the data reached plateau (i.e.
View Article and Find Full Text PDFLongitudinal MRI employing diffusion tensor imaging and T mapping approaches has been applied to investigate the mechanisms of white matter damage caused by acute hexachlorophene neurotoxicity in rats in vivo. Male Sprague-Dawley rats were administered hexachlorophene orally once a day for five consecutive days at a dose of 30mg/kg and were monitored in 7T MRI scanner at days 0 (baseline), 3, 6, 13, and 20 following the first hexachlorophene dose. Quantitative T maps as well as a number of diffusion tensor parameters (fractional anisotropy, radial and axial diffusivity, apparent diffusion coefficient, and trace) were calculated from corresponding MR images.
View Article and Find Full Text PDFThe aim of this study was to assess quantitative changes in T2 relaxation using magnetic resonance imaging approaches in rats exposed to kainic acid to assess the utility of such endpoints as biomarkers of neurotoxicity. Quantitative T2 mapping was performed in 21 rats before and 2, 24, and 48 h after a single ip injection of 10 mg/kg of kainic acid. Three methods of quantifying T2 changes were explored: (1) Thresholding: all voxels exhibiting T2 ≤ 72 ms were designated normal tissue, whereas voxels exhibiting T2 > 72 ms were designated as lesioned tissue; (2) Statistical mapping: T2 maps obtained after treatment were statistically compared with averaged "baseline" maps, voxel-by-voxel; (3) Within-subject difference from baseline: for each individual the baseline T2 map was subtracted from the T2 map obtained after treatment.
View Article and Find Full Text PDFRegul Toxicol Pharmacol
December 2014
MRI was utilized to probe T2 changes in living brain following exposure of rats to one of ten classical neurotoxicants. Brains were subsequently perfused for classical neuropathology examination. This approach was predicated on the assumption that the T2 changes represent loci of neurotoxicity encompassing those seen using neuropathology techniques.
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