Sang-Young Kim1, Hyun-Sung Lee2,
Eunjung Bang2, Hyun-Ju Kim2, Sung-Ho Lee3,
Do-Wan Lee1, Dong-Cheol Woo1, Chi-Bong Choi4,
Bo-Young Choe1
1Department of Biomedical Engineering,
The Catholic University of Korea, Seoul, Korea, Republic of; 2Korea
Basic Science Institute, Korea, Republic of; 3Department of
Veterinary Surgery, Konkuk University, Seoul, Korea, Republic of; 4Department
of Radiology, Kyunghee University Medical Center, Seoul, Korea, Republic of
The
ketamine, a NMDA receptor antagonist, impair prefrontal cortex (PFC) function
in the rat and produce symptoms similar to schizophrenia. In this study, we
used in vivo and in vitro 1H-NMR spectroscopy to examine the brain metabolism
of rat treated with subanesthetic dose of ketamine. In vivo data for Glu/Gln
abnormalities in ketamine-treated rats may support the hypotheses of
glutamate dysfunction for schizophrenia. In addition lower metabolic level of
NAA in rats treated with ketamine may indicate reduced neuronal viability.
Therefore our findings suggest that the neurochemical alterations induced by
ketamine may provide the foundation for pathophysiological models of
schizophrenia.