Krug M, Wagner M, Staak S, Smalla K H
Institute of Pharmacology and Toxicology, Medical Faculty, O.-v-Guericke University, Magdeburg, Germany.
Brain Res. 1994 Apr 18;643(1-2):130-5. doi: 10.1016/0006-8993(94)90018-3.
Male Wistar rats were intrahippocampally injected with L-fucose and the sugar epitope 2'-fucosyl-lactose prior to induction of long-term potentiation (LTP). Both substances had only a minimal and short-lasting depressive effect on the monosynaptically evoked field potential recorded in the dorsal blade of the dentate gyrus of freely moving rats upon stimulation of the perforant pathway. However, LTP induced by fractionated tetanization of the perforant pathway, which declined within 24 h in control animals injected with Lactose, remained at the initial level even 48 h after tetanization (difference to the control group significant with P < 0.01). The results support earlier findings which have indicated a participation of fucosylated macromolecules in the maintenance of LTP. Different molecular mechanisms concerning the effect of both substances and the significance of the data in elucidation of the relationship between LTP and memory formation are discussed.
在诱导长时程增强（LTP）之前，对雄性Wistar大鼠进行海马内注射L-岩藻糖和糖表位2'-岩藻糖基乳糖。在自由活动大鼠的齿状回背叶刺激穿通通路时，记录到的单突触诱发场电位，这两种物质对其仅有轻微且短暂的抑制作用。然而，通过对穿通通路进行分次强直刺激诱导的LTP，在注射乳糖的对照动物中24小时内下降，在强直刺激后48小时仍保持在初始水平（与对照组差异显著，P < 0.01）。这些结果支持了早期的研究发现，即岩藻糖基化大分子参与LTP的维持。讨论了关于这两种物质作用的不同分子机制以及这些数据在阐明LTP与记忆形成之间关系中的意义。
