Mice deficient for the HNK-1 sulfotransferase show alterations in synaptic efficacy and spatial learning and memory

Claudia Senn, Michael Kutsche, Armen Saghatelyan, Michael R. Bösl, Jürgen Löhler, Udo Bartsch, Fabio Morellini, Melitta Schachner

Research output: Contribution to journalArticlepeer-review

71 Scopus citations

Abstract

The HNK-1 carbohydrate structure, a sulfated glucuronyl-lactosaminyl residue carried by many neural recognition molecules, is involved in cell interactions during ontogenetic development and in synaptic plasticity in the adult. To characterize the functional role of the HNK-1 carbohydrate in vivo, we have generated mice deficient for the HNK-1 sulfotransferase (ST). The ST-/- allele is inherited with Mendelian frequencies, and the ST-/- mice are viable and fertile. The anatomy of all major brain areas appeared histologically normal. However, basal synaptic transmission in pyramidal cells in the CA1 region of the hippocampus was increased and long-term potentiation evoked by theta-burst stimulation was reduced in ST mutants. In the water maze, ST-/- mice showed an impaired long-term memory and a poorer spatial learning when a short inter-trial interval was used. These observations indicate an essential role for the sulfate group of the HNK-1 carbohydrate in synaptic plasticity of the hippocampus.

Original languageEnglish (US)
Pages (from-to)712-729
Number of pages18
JournalMolecular and Cellular Neuroscience
Volume20
Issue number4
DOIs
StatePublished - 2002

All Science Journal Classification (ASJC) codes

  • Cellular and Molecular Neuroscience
  • Molecular Biology
  • Cell Biology

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