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短暂性脑缺血大鼠的空间认知障碍及脑内氨基酸、单胺和乙酰胆碱的变化

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

作者信息

Iwasaki K, Kitamura Y, Ohgami Y, Mishima K, Fujiwara M

机构信息

Department of Physiology and Pharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University, Japan.

出版信息

Brain Res. 1996 Feb 19;709(2):163-72. doi: 10.1016/0006-8993(95)01235-4.

Abstract

We investigated the disruption of spatial cognition due to transient forebrain ischemia using an 8-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.

摘要

我们使用大鼠八臂放射状迷宫任务研究了短暂性前脑缺血引起的空间认知障碍。5分钟或10分钟的缺血不影响任务习得。当大鼠通过每日任务训练建立空间认知后,10分钟的缺血在再灌注后24小时执行任务时显著减少了正确选择的数量并增加了错误。然而,经过约4天的每日训练后,这些变化恢复到正常水平。观察到在缺血期间背侧海马(DH)中的谷氨酸(Glu)和乙酰胆碱(ACh)释放短暂增加。然而,在缺血期间,DH中的去甲肾上腺素(NA)含量和NA释放均未改变。然而,DH中的NA和ACh释放在再灌注期间逐渐减少,并且在再灌注后24小时减少变得显著。再灌注7天后,额叶皮质(FC)和DH中的NA含量增加。这些结果表明,10分钟缺血诱导的空间认知障碍在很大程度上可能归因于海马ACh和NA以及皮质NA系统的功能障碍,而不是这些区域神经元细胞死亡的发展。

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