Nakamura M, Hayashi H, Kurata Y, Mitta M, Ohkawa A, Ono K, Shiosaka S, Tohyama M, Esaki K
J Hirnforsch. 1983;24(6):659-70.
To determine the pathomechanism of the condition of CF 1 mutant mice which present paralytic club feet, anatomicohistological analysis (conventional histological staining, silver impregnation, cholinesterase staining, and retrograde tracer technique of horseradish peroxidase (HRP)) were carried out. CF 1 homozygotic mutant mice lacked the common peroneal nerve, while tibial nerve is larger than that of normal mice when they were compared at the similar levels of the posterior limbs. Anterior and lateral crural muscles of the homozygotic mutant mice except for peroneus longus and brevis muscles showed large group muscle atrophy. HRP study indicated that the number of HRP labeled cells after injection of HRP into the anterior and lateral crural muscles decreased remarkably in number in the homozygotic mutant mice, comparing with that of the normal mice.
为了确定呈现麻痹性畸形足的CF 1突变小鼠病症的发病机制，进行了解剖组织学分析（常规组织学染色、银浸染、胆碱酯酶染色以及辣根过氧化物酶（HRP）逆行示踪技术）。当在相似的后肢水平进行比较时，CF 1纯合突变小鼠缺乏腓总神经，而胫神经比正常小鼠的大。纯合突变小鼠除了腓骨长肌和腓骨短肌外的小腿前外侧肌肉呈现大片肌肉萎缩。HRP研究表明，与正常小鼠相比，向纯合突变小鼠的小腿前外侧肌肉注射HRP后，HRP标记细胞的数量显著减少。
