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In Vivo Proton MR Spectroscopy Quantification of Cerebral Neurochemical Changes in Acute Binge Ethanol Exposed Rats

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D Lee

Do-Wan Lee1, Jae-Hwa Kim2, Sang-Young Kim1, Dai-Jin Kim2,3, Jin-Young Jung1, Kyu-Ho Song1, Bo-Young Choe1,*, (1) Department of Biomedical Engineering, and Research Institute of Biomedical Engineering, College of Medicine, The Catholic University of Korea, Seoul, Korea, Republic of, (2) Department of Biomedical Science, The Catholic University of Korea, College of Medicine, Seoul, Korea, Republic of, (3) Department of Psychiatry, Seoul St. Mary's Hospital, The Catholic University of Korea, College of Medicine, Seoul, Korea, Republic of,

SU-E-I-63 Sunday 3:00PM - 6:00PM Room: Exhibit Hall

Purpose:
The cerebral metabolite changes in vivo were quantitatively assessed in binge ethanol₋intoxicated rats by using a 4.7₋T proton magnetic resonance spectroscopy (1H₋MRS).

Methods:
Thirteen 8₋week₋old, male Sprague₋Dawley rats were used and divided into 2 groups (control group: n=6; binge₋ethanol group: n=7). 7 binge ethanol group rats received an initial dose of 5 g/kg (30% w/v solution) via oral gavage method, followed by a maximum dose of 2 g/kg (25% w/v solution) every 8₋h (at 1400, 2200, and 0600) for 4 days. The 6 control group rats simultaneously received equal volumes (about 3.55ml) of normal saline (at 1500, 2300, and 0700). Oral gavage ethanol was administered based on body weight. After 4₋days of oral gavage, in vivo scanning was performed on all animals by using a 4.7₋T Bruker BIOSPEC. The volume of interest (VOI, 6x2x3 mm³; volume: 36 μL; Thirteen water suppressed 1H₋MRS spectra were acquired using PRESS sequences (TR/TE = 4000/20 ms; number of acquisitions = 384; number of data points = 2048).

Results:
Figure 1 shows the representative fitted spectra from hippocampus of binge ethanol and control group rats. Our results showed that total choline (tCho; phosphocholine+glycerophosphocholine [GPC+PCh]) concentrations were significantly lower (p=0.038) in the binge ethanol group than that in the control group (Fig.2). Moreover, tCho/total N₋acetylaspartate (tNAA: NAA+N₋acetylaspartylglutamate [NAAG]) ratios were significantly lower (p=0.043) in the binge₋ethanol group than that in the control group (Fig.3). However, Glutamine/Glutamate ratios showed no significant differences between the 2 groups.

Conclusion:
According to our findings and from results in previous studies, significantly low tCho concentrations and tCho/tNAA ratios may indicate the cell membrane turnover abnormalities of phosphatidylcholine and changed adaptive mechanism in the hippocampus of binge ethanol intoxicated rats. Thus, we provide quantitative in vivo evidence that binge-ethanol exposure causes cerebral neurochemical profile changes in rats, in the hippocampal region.

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