THE AMNESIC SUBSTANCE 2-DEOXY-D-GALACTOSE SUPPRESSES THE MAINTENANCE OF HIPPOCAMPAL LTP
THE AMNESIC SUBSTANCE 2-DEOXY-D-GALACTOSE SUPPRESSES THE MAINTENANCE OF HIPPOCAMPAL LTP
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DOI：
10.1016/0006-8993(91)90513-u
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发表时间：
1991-02-01
期刊：
影响因子：
2.9
通讯作者：
MATTHIES, H
中科院分区：
文献类型：
--
作者：
KRUG, M;JORK, R;MATTHIES, H
雄性Wistar大鼠脑室注射2-脱氧-D-半乳糖（DO-Gal），一种干扰糖大分子岩藻糖基化的物质，在各种学习任务中损害记忆巩固。 发现Do-gal对在穿通通路刺激后记录在齿状回中的单突触诱发场电位（MEFP）没有影响。 然而，海马长时程增强（LTP）诱导的do-gal预处理的动物通过分馏破伤风的穿孔通路下降到对照水平破伤风后2小时，而它保持恒定的24小时，在盐水处理的大鼠。 在海马脑片的CA 1区也观察到类似的效应。 结果表明岩藻糖基化大分子参与了LTP的维持。 讨论了LTP过程对记忆形成的可能意义。
Male Wistar rats were intraventricularly injected with 2-deoxy-D-galactose (do-gal), a substance interfering with the fucosylation of glycomacromolecules and impairing memory consolidation in various learning tasks. Do-gal was found to have no influence on the monosynaptically evoked field potential (MEFP) recorded in the dentate gyrus upon stimulation of the perforant pathway. However, hippocampal long-term potentiation (LTP) induced in do-gal-pretreated animals by fractionated tetanization of the perforant pathway declined to control levels 2 h after tetanization, whereas it remained constant for 24 h in saline-treated rats. Similar effects were observed in the CA1 region of hippocampal slices. The results indicate a participation of fucosylated macromolecules in the maintenance of LTP. The possible significance of processes involved in LTP for memory formation is discussed.