Suppr超能文献

甲钴胺(甲基维生素B12)可促进在薄束轴索性肌萎缩(GAD)突变小鼠薄束前肌中退化的运动神经末梢的再生。

Methylcobalamin (methyl-B12) promotes regeneration of motor nerve terminals degenerating in anterior gracile muscle of gracile axonal dystrophy (GAD) mutant mouse.

作者信息

Yamazaki K, Oda K, Endo C, Kikuchi T, Wakabayashi T

机构信息

Laboratory Animal Research Center, Tsukuba Research Laboratories, Eisai Co., Ltd., Ibaraki, Japan.

出版信息

Neurosci Lett. 1994 Mar 28;170(1):195-7. doi: 10.1016/0304-3940(94)90272-0.

Abstract

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.

摘要

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。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验