Alteration of the sialylation pattern and memory deficits by injection of Aβ(25-35) into the hippocampus of rats

Sialic acid in glycoconjugates participates in important cellular functions associated with normal development, growth, and communication. Therefore we evaluated the sialylation pattern and memory deficits caused by the injection of A beta((25+35)) into the hippocampus (Hp) of rats. The eight-arm maze spatial-learning and memory test indicated that the injection of A beta((25+35)) into subfield CA1 of the Hp impaired both learning and memory. The sialylation pattern was examined using sialic acid-specific lectins. Our results showed that Maackia amurensis agglutinin (MAA, specific for Neu5Ac alpha 2,3Gal) showed reactivity in the CA1 and dentate gyrus (DG) subfields of the Hp mainly in the group injected with vehicle, whereas Macrobrachium rosenbergii lectin (MRL, specific for Neu5,9,7Ac) and Sambucus nigra agglutinin (SNA, specific for Neu5Ac alpha 2,6Gal-GalNAc) had increased reactivity in the CA1 and DG subfields of the Hp in the A beta((25+35))-injected group. The staining pattern of the antibody specific for polysialic acid (a linear homopolymer of alpha-2,8-linked sialic acid) increased in the CA1 and DG subfields of the Hp of the A beta((25+35)) group compared to the control group. Our results suggest that injection of A beta((25+35)) causes impairment in spatial memory and alters the sialylation pattern in response to compensatory reorganization and-or sprouting of dendrites and axons of the surviving neurons. (C) 2011 Elsevier Ireland Ltd. All rights reserved.