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SU‐E‐I‐64: High‐Resolution Detection of Cerebral Neurochemical Profile in Rat Hippocampus After Acute Binge Alcohol Intoxication

Purpose: The aim of present study was to provide ex vivo evidence of changes in neurochemical profiles of rat hippocampus after acute‐binge ethanol intoxication, using high‐resolution magic angle spinning (HR‐MAS) NMR spectroscopy using a 500‐MHz spectrometer. Methods: Twenty‐male‐Wistar rats, divid...

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Published in:Medical Physics 2013-06, Vol.40 (6), p.140-140
Main Authors: Lee, Do‐Wan, Kim, Tai‐Kyung, Shin, Youngwon, Kim, Jae‐Hwa, Kim, Sang‐Young, Jung, Jin‐Young, Song, Kyu‐Ho, Kim, Hwi‐Yool, Kim, Dai‐Jin, Choe, Bo‐Young
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Language:English
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Summary:Purpose: The aim of present study was to provide ex vivo evidence of changes in neurochemical profiles of rat hippocampus after acute‐binge ethanol intoxication, using high‐resolution magic angle spinning (HR‐MAS) NMR spectroscopy using a 500‐MHz spectrometer. Methods: Twenty‐male‐Wistar rats, divided into two groups (control group: n=10, binge ‐ ethanol group: n=10), were used in this study. The 10 rats in binge ‐ ethanol group received an initial ethanol dose of 5 g/kg (30% w/v solution) via oral gavage, then received additional doses of 1.5 g/kg (25% w/v solution) every 8 hours (at 1000, 1800, and 0200 hours) for 4 days. The 10 control rats received an equivalent volume of normal saline, with treatments occurring at comparable times (1100, 1900, and 0300 hours). Ex vivo 1H HR‐MAS spectroscopy was performed using an Agilent VNMRS‐500 (500.13‐MHz). One ‐ dimensional HR‐MAS spectra were acquired from all 20 tissue samples with CPMG sequence [complex data number = 16384, spectral width = 8012.8 Hz, relaxation delay time= 5.0 sec, pre‐saturation time = 2.0 sec, inter‐pulse delay (τ) = 0.4 msec, number of acquisitions = 128, and a total scan time = 15 min 24 sec]. Results: Figure 1 (A and B) shows representative 500‐MHz spectra from hippocampal regions of animals in binge ‐ ethanol and control groups. Figure 2 shows total creatine ratio levels that were quantified from 20 hippocampal tissue samples. Glutamate/tCr (**: p=0.007) and Glx/tCr (Glx: glutamine and glutamate complex [glutamate+glutamine]) (**: p=0.006) ratios were significantly higher in binge‐ethanol group than in control group. Conclusion: Our findings suggest that glutamate signals and glutamate‐glutamine cycle in hippocampal region are particularly sensitive to acute‐binge ethanol consumption. Future studies using a combination of human patients and in vivo animal MRS investigations, as well as other neuroimaging approaches, are required to strengthen our findings and to validate translational component in acute‐binge alcohol intoxicated condition.
ISSN:0094-2405
2473-4209
DOI:10.1118/1.4814174