Nishi M, Kawata M, Azmitia E C
Department of Anatomy and Neurobiology, Kyoto Prefectural University of Medicine, Kamigyou-ku, Japan.
Neurosci Lett. 1997 Jul 4;229(3):212-4. doi: 10.1016/s0304-3940(97)00443-6.
S100beta, 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 S100beta 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 S100beta (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 S100beta rapidly promotes re-assembly and/or stabilization.
S100β是一种由神经胶质细胞产生的、在中枢神经系统具有神经营养活性的钙结合蛋白,可刺激胎儿中缝核、皮质、脊髓和背根神经节神经元的轴突生长。在原代大鼠脊髓培养物中,研究了用秋水仙碱破坏微管后,S100β对轴突长度和微管相关蛋白2(MAP2)免疫反应性(IR)的影响。在用10⁻⁶M秋水仙碱处理30分钟后,再用20 ng/ml S100β孵育3小时,可改变MAP2-IR的分布。与单独秋水仙碱处理相比,MAP2-IR轴突的长度增加了65%。与单独秋水仙碱处理相比,细胞体中MAP2-IR的强度降低了26%。这些结果表明,当微管细胞骨架系统被破坏时,轴突会收缩,而S100β可迅速促进其重新组装和/或稳定。