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Updated: Jul 2, 2026

Whole-mount Imaging of Mouse Embryo Sensory Axon Projections
Published on: December 9, 2014
Sensory neurons from N-syndecan-deficient mice are defective in survival
Mikhail Paveliev1, Anni Hienola, Eija Jokitalo
1Institute of Biotechnology, PO Box 56, Viikki Biocenter, University of Helsinki, Helsinki FIN-00014, Finland. Mikhail.Paveliev@helsinki.fi
Abstract:
Extracellular matrix is a crucial regulator of development, plasticity and regeneration in the nervous system. We have now found that N-syndecan, the receptor for the extracellular matrix component heparin-binding growth-associated molecule, is required for survival of primary sensory neurons. We demonstrate massive cell death of cultured dorsal root ganglion (DRG) neurons from mice deficient in the N-syndecan gene as compared with wild-type controls. Importantly, this cell death could not be prevented by nerve growth factor - the neurotrophin, which activates multiple antiapoptotic cascades in DRG neurons. The survival deficiency was observed during first postnatal week. In contrast, DRG neurons from young adult N-syndecan knockout mice exhibited normal survival. This study identifies a completely new syndecan-dependent type of signaling that regulates cell death in neurons.

