Ishimaru H, Takahashi A, Ikarashi Y, Maruyama Y
Department of Neuropsychopharmacology (Tsumura), Gunma University School of Medicine, Japan.
Brain Res. 1994 Mar 7;639(1):66-72. doi: 10.1016/0006-8993(94)91765-5.
Temporal changes in cholinergic functions following transient cerebral ischemia (10 min) were studied in the hippocampus of awake unrestrained gerbils using in vivo microdialysis. These data were compared with the results for temporal change in the area of each CA1 cell soma, measured with a microcomputer imaging device. KCl-induced release of acetylcholine (ACh) tended to be lower within 1 day after recirculation, and was significantly lower on the 4th, 7th and 14th days. Atropine-induced release of ACh gradually decreased over the test period. In histological estimation, no differences were observed within the 1st day, but a significant decrease of the area of CA1 cell soma was observed from the 4th to 14th days. Moreover, ischemia over 2 min decreased KCl- and atropine-induced ACh release on the 14th day without significant changes of hippocampal CA1 pyramidal cell. From these results, it is clear that ischemia produced dysfunction of hippocampal cholinergic neurons, and that dysfunction of the hippocampal cholinergic system following transient ischemia precedes pyramidal cell damage in the hippocampal CA1 subfield.
使用体内微透析技术，对清醒无束缚沙鼠海马体中短暂性脑缺血（10分钟）后胆碱能功能的时间变化进行了研究。将这些数据与用微型计算机成像设备测量的每个CA1细胞体面积的时间变化结果进行了比较。再灌注后1天内，氯化钾诱导的乙酰胆碱（ACh）释放趋于降低，在第4、7和14天显著降低。在测试期间，阿托品诱导的ACh释放逐渐减少。在组织学评估中，第1天内未观察到差异，但从第4天到第14天观察到CA1细胞体面积显著减小。此外，超过2分钟的缺血在第14天降低了氯化钾和阿托品诱导的ACh释放，而海马CA1锥体细胞无明显变化。从这些结果可以清楚地看出，缺血导致海马胆碱能神经元功能障碍，短暂性缺血后海马胆碱能系统功能障碍先于海马CA1亚区锥体细胞损伤。
