High-Resolution Detection of Cerebral Neurochemical Profile in Rat Hippocampus After Acute Binge Alcohol Intoxication
Do-Wan Lee1, Tai-Kyung Kim2, Youngwon Shin2, Jae-Hwa Kim3, Sang-Young Kim1, Jin-Young Jung1, Kyu-Ho Song1, Hwi-Yool Kim2, Dai-Jin Kim3,4, 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 Veterinary Surgery, Konkuk University of Korea, Seoul, Korea, Republic of, (3) Department of Biomedical Science, The Catholic University of Korea, College of Medicine, Seoul, Korea, Republic of, (4) Department of Psychiatry, Seoul St. Mary's Hospital, The Catholic University of Korea, College of Medicine, Seoul, South KoreaSU-E-I-64 Sunday 3:00PM - 6:00PM Room: Exhibit Hall
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.
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].
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.
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.