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Scientific article
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Brain-derived neurotrophic factor restores long-term potentiation in polysialic acid-neural cell adhesion molecule-deficient hippocampus

Publication date2000
Abstract

The neural cell adhesion molecule (NCAM) and its polysialylated form (PSA-NCAM) contribute to long-term potentiation (LTP) in the CA1 hippocampus. Here we report that the deficient LTP found in slices prepared from NCAM knockout mice and in organotypic slice cultures treated with Endo-N, an enzyme that cleaves the PSA moiety of NCAM, can be rescued by brain-derived neurotrophic factor (BDNF). This effect is not reproduced by nerve growth factor, but can be obtained with high concentrations of NT4/5. The effect of BDNF cannot be accounted for by modifications of N-methyl-D-aspartate receptor-dependent responses or of high-frequency bursts. PSA-NCAM, however, could directly interact with BDNF. Exogenous application of PSA residues or recombinant PSA-NCAM also prevents LTP. Furthermore trkB phosphorylation, and thus BDNF signaling, is reduced in both NCAM knockout mice and Endo-N-treated slice cultures. These results suggest that one action of PSA-NCAM could be to sensitize pyramidal neurons to BDNF, thereby modulating activity-dependent synaptic plasticity.

Keywords
  • Animals
  • Brain-Derived Neurotrophic Factor/ physiology
  • Culture Techniques
  • Hippocampus/metabolism/ physiology
  • Long-Term Potentiation/ physiology
  • Mice
  • Mice, Knockout
  • Neural Cell Adhesion Molecules/ genetics
  • Phosphorylation
  • Rats
  • Rats, Sprague-Dawley
  • Receptor, trkB/metabolism
Citation (ISO format)
MULLER, Dominique et al. Brain-derived neurotrophic factor restores long-term potentiation in polysialic acid-neural cell adhesion molecule-deficient hippocampus. In: Proceedings of the National Academy of Sciences of the United States of America, 2000, vol. 97, n° 8, p. 4315–4320. doi: 10.1073/pnas.070022697
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ISSN of the journal0027-8424
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