In Vivo Measurement of Neurochemical Abnormalities in the Hippocampus in a Rat Model of Cuprizone-Induced Demyelination

被引:6
作者
Lee, Do-Wan [1 ]
Kwon, Jae-Im [2 ]
Woo, Chul-Woong [2 ]
Heo, Hwon [3 ]
Kim, Kyung Won [1 ]
Woo, Dong-Cheol [2 ,3 ]
Kim, Jeong Kon [1 ]
Lee, Dong-Hoon [4 ]
机构
[1] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Radiol, Seoul 05505, South Korea
[2] Asan Med Ctr, Asan Inst Life Sci, Convergence Med Res Ctr, Seoul 05505, South Korea
[3] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Convergence Med, Seoul 05505, South Korea
[4] Yonsei Univ, Dept Radiat Convergence Engn, Wonju 26493, South Korea
基金
新加坡国家研究基金会;
关键词
rat brain; demyelination; hippocampus; metabolites; multiple sclerosis;
D O I
10.3390/diagnostics11010045
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
This study quantitatively measured the changes in metabolites in the hippocampal lesions of a rat model of cuprizone-induced demyelination as detected using in vivo 7 T proton magnetic resonance spectroscopy. Nineteen Sprague Dawley rats were randomly divided into two groups and fed a normal chow diet or cuprizone (0.2%, w/w) for 7 weeks. Demyelinated hippocampal lesions were quantitatively measured using a 7 T magnetic resonance imaging scanner. All proton spectra were quantified for metabolite concentrations and relative ratios. Compared to those in the controls, the cuprizone-induced rats had significantly higher concentrations of glutamate (p = 0.001), gamma-aminobutyric acid (p = 0.019), and glutamate + glutamine (p = 0.001); however, creatine + phosphocreatine (p = 0.006) and myo-inositol (p = 0.001) concentrations were lower. In addition, we found that the glutamine and glutamate complex/total creatine (p < 0.001), glutamate/total creatine (p < 0.001), and GABA/total creatine (p = 0.002) ratios were significantly higher in cuprizone-treated rats than in control rats. Our results showed that cuprizone-induced neuronal demyelination may influence the severe abnormal metabolism in hippocampal lesions, and these responses could be caused by microglial activation, mitochondrial dysfunction, and astrocytic necrosis.
引用
收藏
页数:10
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