Brain Res. 1991 Feb 1;540(1-2):237-42.

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

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

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

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.

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