The disruption of spatial cognition and changes in brain amino acid, monoamine and acetylcholine in rats with transient cerebral ischemia

被引:46
作者
Iwasaki, K [1 ]
Kitamura, Y [1 ]
Ohgami, Y [1 ]
Mishima, K [1 ]
Fujiwara, M [1 ]
机构
[1] FUKUOKA UNIV,FAC PHARMACEUT SCI,DEPT PHYSIOL & PHARMACOL,FUKUOKA 81480,JAPAN
关键词
cerebral ischemia; spatial cognition; 8-Arm radial maze task; microdialysis; glutamate; noradrenaline; acetylcholine; DELAYED NEURONAL DEATH; FOREBRAIN ISCHEMIA; GERBIL HIPPOCAMPUS; GLUTAMATE; DAMAGE; MODEL; MEMORY;
D O I
10.1016/0006-8993(95)01235-4
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
We investigated the disruption of spatial cognition due to transient forebrain ischemia using an B-arm radial arm maze task in rats. Five or 10 min of ischemia did not affect the task acquisition. When rats established spatial cognition by daily training of the task, 10 min of ischemia significantly decreased the number of correct choices and increased the errors in the task when performed 24 h after reperfusion. These changes, however, returned to the normal level after about 4 days of daily training. Glutamic acid (Glu) and acetylcholine (ACh) release from the dorsal hippocampus (DH) was observed to transiently increase during ischemia. However, neither the content of noradrenaline (NA) nor the release of NA in the DH changed during ischemia. The NA and ACh release from the DH, however, gradually decreased during reperfusion, and the decrease became significant at 24 h after reperfusion. The NA content of the frontal cortex (FC) and the DH increased 7 days after reperfusion. These results suggest that the disruption of spatial cognition induced by 10 min of ischemia may be attributed to a greater degree to the dysfunction of the hippocampal ACh and NA, and cortical NA systems, rather than to the development of neuronal cell death in these areas.
引用
收藏
页码:163 / 172
页数:10
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