Uemura E, Levin E D, DeLuna R, Bowman R E
Department of Anatomy, Iowa State University, Ames 50011.
Brain Res. 1989 Sep 4;496(1-2):317-20. doi: 10.1016/0006-8993(89)91080-9.
Reactive synaptogenesis was studied in the dentate gyrus of rats exposed to 100 parts per million of halothane for 15 days starting on the day after unilateral entorhinal lesioning. Halothane exposure markedly affected the replacement of synapses. Only 17% of the lost synapses were restored by day 15 postlesion in rats exposed to halothane, while 73% of the lost synapses were recovered in rats not exposed to halothane. However, this suppression in initial reactive synaptogenesis did not result in permanent deficits in synaptic population. After halothane exposure was stopped, reactive synaptogenesis resumed, and by day 30 after the lesion, the synaptic population of the experimental group caught up to the control level. This suppressive action of halothane suggests its utility as a research tool for delaying synaptogenesis during selected developmental epochs to study the relationship between synaptic and behavioral recovery.
从单侧内嗅皮层损伤后的第二天开始,对暴露于百万分之一百浓度氟烷环境中15天的大鼠齿状回进行反应性突触形成的研究。氟烷暴露显著影响突触的替代。在暴露于氟烷的大鼠中,损伤后第15天仅17%的丢失突触得以恢复,而未暴露于氟烷的大鼠中73%的丢失突触得以恢复。然而,这种对初始反应性突触形成的抑制并未导致突触数量的永久性缺陷。停止氟烷暴露后,反应性突触形成恢复,损伤后第30天,实验组的突触数量赶上了对照组水平。氟烷的这种抑制作用表明其作为一种研究工具,可用于在特定发育阶段延迟突触形成,以研究突触与行为恢复之间的关系。