失忆物质2-脱氧-D-半乳糖会抑制海马体LTP的维持。

The amnesic substance 2-deoxy-D-galactose suppresses the maintenance of hippocampal LTP.

作者信息

Krug M, Jork R, Reymann K, Wagner M, Matthies H

机构信息

Institute of Pharmacology and Toxicology, Medical Academy, Magdeburg, Germany.

出版信息

Brain Res. 1991 Feb 1;540(1-2):237-42. doi: 10.1016/0006-8993(91)90513-u.

DOI:10.1016/0006-8993(91)90513-u

PMID:2054616

Abstract

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.

摘要

雄性Wistar大鼠经脑室注射2-脱氧-D-半乳糖（do-gal），该物质会干扰糖大分子的岩藻糖基化，并损害各种学习任务中的记忆巩固。研究发现，do-gal对刺激穿通通路时在齿状回记录的单突触诱发场电位（MEFP）没有影响。然而，在经do-gal预处理的动物中，通过对穿通通路进行分次强直刺激诱导的海马长时程增强（LTP）在强直刺激后2小时下降至对照水平，而在生理盐水处理的大鼠中，LTP在24小时内保持恒定。在海马切片的CA1区域也观察到了类似的效果。结果表明岩藻糖基化大分子参与了LTP的维持。文中还讨论了LTP相关过程对记忆形成的可能意义。