Aniracetam enhances glutamatergic transmission in the prefrontal cortex of stroke-prone spontaneously hypertensive rats

被引:11
作者
Togashi, H
Nakamura, K
Matsumoto, M
Ueno, K
Ohashi, S
Saito, H
Yoshioka, M
机构
[1] Hokkaido Univ, Grad Sch Med, Dept Pharmacol, Kita Ku, Sapporo, Hokkaido 0608638, Japan
[2] Nippon Roche Res Ctr, CNS Supporting Lab, Kamakura, Kanagawa 2478530, Japan
[3] Japanese Red Cross Hokkaido Coll Nursing, Dept Basic Sci, Kitami, Hokkaido 0900011, Japan
关键词
prefrontal cortex; amygdala; aniracetam glutamate; gamma-aminobutyric acid; nitric oxide; stroke-prone spontaneously hypertensive rats;
D O I
10.1016/S0304-3940(01)02436-3
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The effects of aniracetam, a cognition enhancer, on extracellular levels of glutamate (Glu), gamma-aminobutyric acid (GABA) and nitric oxide metabolites (NOx) were examined in the prefrontal cortex (PFC) and the basolateral amygdala (AMG) in stroke-prone spontaneously hypertensive rats (SHRSP) using in vivo microdialysis. Basal release of Glu, was lower in the AMG of SHRSP than in normotensive Wistar Kyoto rats, whereas no difference in GABA and NOx was noted. Aniracetam (100 mg/kg, p.o.) significantly increased the area under the curve of Glu levels in the PFC, but not in the AMG, of SHRSP. Aniracetam failed to exert any remarkable effects on GABA or NOx levels in either brain region. Our findings suggest that aniracetam enhances cortical glutamatergic release, which may be the mechanism involved in the ameliorating effects of aniracetam on various neuronal dysfunctions. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.
引用
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页码:109 / 112
页数:4
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