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Alterations of plasma and cerebrospinal fluid glutamate levels in rats treated with the N ‐methyl‐ D ‐aspartate receptor antagonist, ketamine
Author(s) -
Tomiya Masayuki,
Fukushima Takeshi,
Kawai Junko,
Aoyama Chiaki,
Mitsuhashi Shogo,
Santa Tomofumi,
Imai Kazuhiro,
Toyo'oka Toshimasa
Publication year - 2006
Publication title -
biomedical chromatography
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.4
H-Index - 65
eISSN - 1099-0801
pISSN - 0269-3879
DOI - 10.1002/bmc.677
Subject(s) - chemistry , cerebrospinal fluid , nmda receptor , glutamate receptor , ketamine , antagonist , pharmacology , receptor , receptor antagonist , anesthesia , medicine , biochemistry
It has been reported that the repeated administration of a sub‐anesthetic dose of an N ‐methyl‐ D ‐aspartate receptor antagonist, ketamine, can produce an animal model of schizophrenia. Since no information is available on the alterations of the amino acid levels in ketamine‐treated rats, we investigated the amino acid composition in the plasma and cerebrospinal fluid of rats that were repeatedly administered with ketamine for 5 consecutive days (30 mg/kg/day). The plasma and cerebrospinal fluid amino acid compositions in the fifth week after cessation of repeated ketamine administration were determined by highperformance liquid chromatography with fluorescence detection using a pre‐column fluorescence reagent, i.e. 4‐fluoro‐7nitro‐2,1,3‐benzoxadiazole. Among the amino acids investigated in the present study, the level of plasma glutamic acid increased significantly ( p < 0.05), while that of the cerebrospinal fluid glutamic acid decreased significantly in the ketamine‐treated rats as compared with these levels in control rats injected with saline ( p < 0.05, n = 7). These alterations in the glutamic acid level in the plasma and cerebrospinal fluid resemble those in schizophrenic patients, suggesting that ketamine‐treated rats may be a useful model for performing research on the pathophysiology of schizophrenia. Copyright © 2006 John Wiley & Sons, Ltd.