S100 β promotes the extension of microtubule associated protein2 (MAP2)-immunoreactive neurites retracted after colchicine treatment in rat spinal cord culture

• Published in: Neuroscience letters 1997-07, Vol.229 (3), p.212-214
• Main Authors: Nishi, Mayumi, Kawata, Mitsuhiro, Azmitia, Efrain C
• Format: Article
• Language: English
• Subjects: Biological and medical sciences; Cell structures and functions; Cytoskeleton, cytoplasm. Intracellular movements; Depolymerization; Fundamental and applied biological sciences. Psychology; Microtubular cytoskeletal system; Molecular and cellular biology; Phosphorylation; Polymerization; Primary culture; Spinal cord injury
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/S0304-3940(97)00443-6

S100 β, a glial derived calcium-binding protein with neurotrophic activity in the central nervous system, stimulates neurite extension of fetal raphe, cortex, spinal cord, and dorsal root ganglion neurons. The effects of S100 β on neurite length and microtubule associated protein2 (MAP2) immunoreactivity (IR) after microtubule disruption with colchicine were investigated in primary rat spinal cord culture. The incubation with S100 β (20 ng/ml) for 3 h after exposure to colchicine (10 −6 M) for 30 min altered the distribution of MAP2-IR. The length of MAP2-IR neurites increased by 65% compared to that in colchicine treatment alone. MAP2-IR intensity in the cell body was reduced by 26% compared to that in colchicine treatment alone. These results indicate that neurites shrink when the microtubular cytoskeletal system is disrupted and S100 β rapidly promotes re-assembly and/or stabilization.