Sensory neurons from N-syndecan-deficient mice are defective in survival

• Published in: Neuroreport Vol. 19; no. 14; p. 1397
• Main Authors: Paveliev, Mikhail, Hienola, Anni, Jokitalo, Eija, Planken, Anu, Bespalov, Maxim M, Rauvala, Heikki, Saarma, Mart
• Format: Journal Article
• Language: English
• Published: England 17.09.2008
• Subjects: Animals; Carrier Proteins - genetics; Cell Death; Cell Survival - drug effects; Cell Survival - physiology; Cells, Cultured; Cytokines - genetics; Ganglia, Spinal - cytology; Glial Cell Line-Derived Neurotrophic Factor - pharmacology; Growth Cones - drug effects; Growth Cones - metabolism; Immunohistochemistry; Mice; Mice, Inbred C57BL; Mice, Knockout; Nerve Growth Factor - pharmacology; Neurons, Afferent - cytology; Neurons, Afferent - metabolism; Neurons, Afferent - physiology; Neurturin - pharmacology; Receptor, trkA - genetics; Reverse Transcriptase Polymerase Chain Reaction; Signal Transduction - drug effects; Signal Transduction - physiology; Syndecans - deficiency; Syndecans - genetics
• ISSN: 1473-558X
• DOI: 10.1097/WNR.0b013e32830d1486

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.