Yamazaki K, Oda K, Endo C, Kikuchi T, Wakabayashi T
Laboratory Animal Research Center, Tsukuba Research Laboratories, Eisai Co., Ltd., Ibaraki, Japan.
Neurosci Lett. 1994 Mar 28;170(1):195-7. doi: 10.1016/0304-3940(94)90272-0.
We examined the effects of methylcobalamin (methyl-B12, mecobalamin) on degeneration of motor nerve terminals in the anterior gracile muscle of gracile axonal dystrophy (GAD) mutant mice. GAD mice received orally methyl-B12 (1 mg/kg body wt/day) from the 40th day after birth for 25 days. In the distal endplate zone of the muscle, although most terminals were degenerated in both the untreated and methyl-B12-treated GAD mice, sprouts were more frequently observed in the latter. In the proximal endplate zone, where few degenerated terminals were seen in both groups of the mice, the perimeter of the terminals was increased and the area of the terminals was decreased significantly in the methyl-B12-treated GAD mice. These findings indicate that methyl-B12 promotes regeneration of degenerating nerve terminals in GAD mice.
我们研究了甲钴胺(甲基维生素B12、甲钴胺)对薄束轴索性肌萎缩(GAD)突变小鼠薄束肌前运动神经末梢变性的影响。GAD小鼠从出生后第40天起口服甲基维生素B12(1毫克/千克体重/天),持续25天。在肌肉的远端终板区,尽管未治疗和甲基维生素B12治疗的GAD小鼠中大多数终末都发生了变性,但在后者中更频繁地观察到芽生。在近端终板区,两组小鼠中均未见变性终末,在甲基维生素B12治疗的GAD小鼠中,终末的周长增加而面积显著减小。这些发现表明,甲基维生素B12促进GAD小鼠变性神经末梢的再生。