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The Journal of Neuroscience, July 15, 2000, 20(14):5234-5244
Mice Deficient in the Polysialyltransferase ST8SiaIV/PST-1 Allow
Discrimination of the Roles of Neural Cell Adhesion Molecule Protein
and Polysialic Acid in Neural Development and Synaptic
Plasticity
Matthias
Eckhardt1,
Olena
Bukalo3,
Geneviève
Chazal2,
Lihua
Wang1,
Christo
Goridis2,
Melitta
Schachner3,
Rita
Gerardy-Schahn1,
Harold
Cremer2, and
Alexander
Dityatev3
1 Institut für Medizinische Mikrobiologie,
Medizinische Hochschule Hannover, D-30625 Hannover, Germany,
2 Laboratoire de Génétique et Physiologie du
Développement, IBDM, Centre National de la Recherche
Scientifique, Institut National de la Santé et de la Recherche
Médicale, Université de la Méditerranée,
F-13288 Marseille, France, and 3 Zentrum für
Molekulare Neurobiologie, Universität Hamburg, D-20246 Hamburg,
Germany
Functional properties of the neural cell adhesion molecule
(NCAM) are strongly influenced by polysialylation. We used
gene-targeting to generate mice lacking ST8SiaIV/PST-1, one of the
polysialyltransferases responsible for addition of polysialic acid
(PSA) to NCAM. Mice homozygous for the null mutation reveal normal
development of gross anatomical features. In contrast to NCAM-deficient
mice, olfactory precursor cells in the rostral migratory stream express PSA and follow their normal pathway. Furthermore, delamination of mossy
fibers in the hippocampal CA3 region, as found in NCAM-deficient mice,
does not occur in ST8SiaIV mutants. However, during postnatal development these animals show a decrease of PSA in most brain regions
compared to wild-type animals. Loss of PSA in the presence of NCAM
protein but in the absence of obvious histological changes allowed us
to directly address the role of PSA in synaptic plasticity. Schaffer
collateral-CA1 synapses, which express PSA in wild types, showed
impaired long-term potentiation (LTP) and long-term depression (LTD) in
adult mutants. This impairment was age-dependent, following the time
course of developmental disappearance of PSA. Contrary to NCAM mutant
mice, LTP in ST8SiaIV mutants was undisturbed at mossy fiber-CA3
synapses, which do not express PSA in wild-type mice. The results
demonstrate an essential role for ST8SiaIV in synaptic plasticity in
hippocampal CA1 synapses, whereas PSA produced by different
polysialyltransferase or polysialyltransferases at early stages of
differentiation regulates migration of neural precursor cells and
correct lamination of mossy fibers. We suggest that NCAM but not PSA is
likely to be important for LTP in the hippocampal CA3 region.
Key words:
gene targeting; hippocampus; long-term potentiation; long-term depression; neural cell adhesion molecule; polysialic acid; polysialyltransferase
Copyright © 2000 Society for Neuroscience 0270-6474/00/20145234-11$05.00/0
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